@article {pmid42772330,
year = {2026},
author = {Liu, L and Kazemian, E and Loroña, NC and Shirazipour, C and Gong, J and Crowder, SL and Nguyen, N and Damerell, V and Mooney, K and Playdon, MC and Ulrich, CM and Li, CI and Shibata, D and Toriola, AT and Ose, J and Peoples, AR and Hardikar, S and Siegel, EM and Bower, JE and Gigic, B and Hoogland, AI and Li, X and Small, BJ and Kaufman, H and Jim, HSL and Figueiredo, JC},
title = {Longitudinal Study on the Influence of Physical Activity in Managing Fatigue in Patients With Colorectal Cancer.},
journal = {Journal of the National Comprehensive Cancer Network : JNCCN},
volume = {},
number = {},
pages = {1-8},
doi = {10.6004/jnccn.2026.7035},
pmid = {42772330},
issn = {1540-1413},
abstract = {BACKGROUND: Fatigue is a prevalent and debilitating symptom among patients with cancer. Physical activity (PA) may help reduce fatigue and improve quality of life (QoL). This study evaluated longitudinal associations between PA, fatigue, and QoL across the cancer care continuum.

METHODS: Data were analyzed from 1,718 participants in a prospective multicenter cohort. Self-reported PA was assessed at baseline and up to 24 months post-diagnosis using a questionnaire based on the International PA Questionnaire (IPAQ). Metabolic equivalent task (MET)-minutes per week were calculated for walking, moderate, vigorous, and total physical activity. Fatigue and QoL were measured using the EORTC Quality of Life Questionnaire-Core 30 (QLQ-C30). Mixed-effects models evaluated associations between PA and outcomes. Lagged fluctuation models examined temporal relationships, separating between-person and within-person effects.

RESULTS: PA levels increased steadily from diagnosis through 24 months, coinciding with reduced fatigue and improved QoL. Higher PA was consistently linked to better fatigue and QoL outcomes. Walking was associated with lower odds of severe fatigue at 6 months (odds ratio [OR], 0.78; 95% CI, 0.62-0.98; P=.031) and 12 months (OR, 0.74; 95% CI, 0.59-0.94; P=.014), with higher odds of better QoL at all follow-up points. Vigorous activity showed the strongest protective effect against fatigue at 24 months (OR, 0.65; 95% CI, 0.45-0.94; P=.023). In patients with nonmetastatic disease, protective associations were observed across all activity types and time points. Lagged models indicated that higher average vigorous activity predicted lower future fatigue (P<.001).

CONCLUSIONS: Greater PA, particularly walking, was associated with lower fatigue and improved QoL, especially in patients with early-stage disease. The posttreatment period (approximately 1 year post-diagnosis) may represent an important window for behavioral intervention. Findings support stage- and recovery phase-specific guidance and highlight walking as a scalable, low-risk target for survivorship care.},
}

@article {pmid42772761,
year = {2026},
author = {Cespedes Feliciano, EM and Fuller, SE and Nugent, JR and Cao, A and Anderson, GL and Paskett, ED and Caan, BJ and Banack, HR and Presley, CJ and Carroll, JE and Manson, JE and Shadyab, AH and Binder, AM},
title = {Lifestyle and chemotherapy shape functional aging trajectories in older breast cancer survivors and matched comparators.},
journal = {Journal of the National Cancer Institute},
volume = {},
number = {},
pages = {},
doi = {10.1093/jnci/djag292},
pmid = {42772761},
issn = {1460-2105},
support = {R01CA283839//the National Cancer Institute at the National Institutes of Health/ ; 75N92021D00001, 75N92021D00002, 75N92021D00003, 75N92021D00004, and 75N92021D00005//the National Heart, Lung, and Blood Institute, National Institutes of Health, U.S. Department of Health and Human Services/ ; UM1 CA173642//The WHI Life and Longevity after Cancer (LILAC) study/ ; },
abstract = {BACKGROUND: Breast cancer and its treatment may contribute to premature aging, but long-term evidence regarding risk factors for functional decline is limited among the growing population of older survivors.

METHODS: In the Women's Health Initiative (n = 45 530; median age at index or diagnosis = 72 years), we compared repeated RAND Short Form 36 (SF-36) physical function scores (0-100) among women with localized (n = 6462) or regional breast cancer (n = 1872) to age-matched, cancer-free comparators (n = 37 196) over 15 years. We tested effect modification by treatment (including agent class), age, and prediagnosis lifestyle behaviors (diet, physical activity, and smoking). Physical performance (grip strength, walking pace) was evaluated in a subset (1045 survivors; 1970 comparators).

RESULTS: Survivors experienced acute postdiagnosis declines followed by incomplete recovery leading to a persistent SF-36 deficit relative to age-matched comparators. Regional disease showed larger deficits (-6.8 at year 1; -5.3 at year 10), with the steepest early declines among chemotherapy recipients (-7.1 at year 1), consistent across agents. Grip strength and walking pace showed trends similar to SF-36 deficits. Deficits relative to cancer-free comparators were greater and sustained among older individuals, whereas those aged younger than 70 years showed lesser differences after an early postdiagnosis drop. Among women with lower-risk lifestyle, survivors remained lower than comparators early after diagnosis but showed greater recovery over time; women with higher-risk lifestyles had persistently lower function overall with lesser differences by cancer status.

CONCLUSIONS: Breast cancer, especially with chemotherapy, was associated with durable functional deficits among older women. Healthier prediagnosis lifestyles are associated with greater functional reserve and better recovery trajectories, suggesting intervention targets for aging survivors.},
}

@article {pmid42775648,
year = {2026},
author = {Etzioni, R and Kessler, L and Schrag, D and Sasieni, P and Robbins, HA and Katki, HA and Duffy, SW and Gulati, R and Buist, D and Tunis, S and Landy, R and Lange, J and Patel, AV and Dahut, WL and Smith, RA},
title = {Recommendations of the American Cancer Society workshop on design, conduct, analysis, and reporting of multicancer early detection trials with late-stage incidence end points and post-trial ongoing evaluation-The Peachtree Consensus.},
journal = {Cancer},
volume = {132},
number = {19},
pages = {e70628},
pmid = {42775648},
issn = {1097-0142},
support = {UG1 CA286954/CA/NCI NIH HHS/United States ; R50 CA221836/CA/NCI NIH HHS/United States ; U24 CA086368/CA/NCI NIH HHS/United States ; R35 CA274442/CA/NCI NIH HHS/United States ; //American Cancer Society/ ; },
mesh = {Humans ; *Neoplasms/diagnosis/epidemiology/pathology ; *Early Detection of Cancer/methods/standards ; American Cancer Society ; United States ; Incidence ; *Research Design ; *Clinical Trials as Topic/standards ; },
abstract = {BACKGROUND: In a new era of multicancer early detection (MCED), late-stage incidence has been proposed as an end point for the evaluation of test efficacy, marking a departure from the established end point of cancer mortality.

METHODS: The American Cancer Society convened a panel of 15 academic researchers with expertise in cancer screening evaluation to develop principles assuring the validity and interpretability of MCED trials with late-stage incidence end points and advancing implementation of tests with potential for meaningful clinical utility.

RESULTS: The definition of late-stage cancer is critical and affects study design, interpretation, and outcomes. The authors of the Peachtree Consensus recommend considering cancer-type-specific definitions of late stage and paying attention to comparability of staging intensity in both trial arms. The duration of screening and the follow-up interval after the last screen should be chosen based on the preclinical early stage and late-stage durations of the target cancer types. The authors also recommend reporting aggregate results and results for individual cancer types as numbers permit and summarizing relative and absolute benefits. Predicted mortality reductions should be calculated to contextualize a late-stage result and the inputs and assumptions involved should be reported. Given a significant late-stage reduction suggestive of meaningful clinical benefit, the authors support launching consortium and demonstration studies while continuing to track trial mortality outcomes.

CONCLUSIONS: Trials with late-stage incidence end points that are conducted using these principles should support the development of evidence-based screening guidelines as well as the creation of accessible data resources for observational and modeling studies.},
}

Humans
*Neoplasms/diagnosis/epidemiology/pathology
*Early Detection of Cancer/methods/standards
American Cancer Society
United States
Incidence
*Research Design
*Clinical Trials as Topic/standards

@article {pmid42776062,
year = {2026},
author = {Shoghi, KI and Badea, CT and Peehl, DM and Chenevert, TL and Daldrup-Link, HE and Hawkins, DS and Houghton, AM and Kinahan, PE and Lewis, MT and Ma, CX and Manning, HC and Miyaoka, RS and Mowery, YM and O'Connor, JP and O'Dwyer, PJ and Ross, BD and Sriram, R and Yankeelov, TE and Zhou, R and Kurhanewicz, J and Mankoff, DA},
title = {The Next Frontier in Quantitative Co-Clinical Imaging to Advance Functional Precision Oncology.},
journal = {Clinical cancer research : an official journal of the American Association for Cancer Research},
volume = {},
number = {},
pages = {},
pmid = {42776062},
issn = {1557-3265},
support = {P41 EB013598/EB/NIBIB NIH HHS/United States ; U54 CA224076/CA/NCI NIH HHS/United States ; U24 CA220245/CA/NCI NIH HHS/United States ; P30 CA015704/CA/NCI NIH HHS/United States ; U24 CA226110/CA/NCI NIH HHS/United States ; U24 CA220325/CA/NCI NIH HHS/United States ; P50 CA236733/CA/NCI NIH HHS/United States ; U10 CA180886/CA/NCI NIH HHS/United States ; P50 CA228944/CA/NCI NIH HHS/United States ; R01 CA273194/CA/NCI NIH HHS/United States ; R01 CA238023/CA/NCI NIH HHS/United States ; R01 CA297995/CA/NCI NIH HHS/United States ; U24 CA209837/CA/NCI NIH HHS/United States ; U24 CA253531/CA/NCI NIH HHS/United States ; U24 CA253377/CA/NCI NIH HHS/United States ; U24 CA231858/CA/NCI NIH HHS/United States ; P30 CA091842/CA/NCI NIH HHS/United States ; U24 CA264044/CA/NCI NIH HHS/United States ; U24 CA237683/CA/NCI NIH HHS/United States ; R01 CA302738/CA/NCI NIH HHS/United States ; U10 CA180899/CA/NCI NIH HHS/United States ; },
abstract = {Precision oncology seeks to transform cancer treatment into one tailored for individual patients. Genomic alterations have been the dominant drivers of patient-specific therapeutic strategies. While genomic insights can guide treatment planning, genotype-directed therapies do not guarantee response to therapy. Functional confirmation of target expression, target engagement, and downstream biological effects is essential to defining therapeutic endpoints. Translational imaging can play a central role in closing the loop between genome and function to operationalize functional precision medicine (FPM). Quantitative co-clinical imaging provides a powerful framework to link genotype with function by confirming drug delivery, target engagement, pharmacodynamic effects, tumor function and heterogeneity across animal models and patients to advance FPM. Over the past decade, the Co-Clinical Imaging Research Resource Program (CIRP) of the National Cancer Institute (NCI) has made considerable progress in advancing quantitative imaging biomarker development. However, critical gaps remain in the integration and standardization of co-clinical imaging biomarkers. The next frontier requires moving beyond quantitative endpoints toward predictive oncology. This includes validating imaging-aware models, developing quantitative imaging strategies to support new precision medicine trials, and embedding co-clinical data into computational and in silico frameworks such as radiomics, cross-species mathematical modeling, digital twins, and virtual imaging trials. Equally important is the development of a domain-specific repository that vertically integrates imaging with multi-modal data to enable reproducible, artificial intelligence-ready pipelines. These advances will accelerate the translation of co-clinical imaging biomarkers into decision models that complement genomics, improve patient stratification, and guide selection and personalization of therapies-advancing the promise of FPM.},
}

@article {pmid42777623,
year = {2026},
author = {Cigliola, A and Dizman, N and Mercinelli, C and Zhu, Y and Carlo, MI and Psutka, SP and Berg, SA and Prakash, G and Aragon-Ching, JB and Oualla, K and Linville, LM and Nguyen, CB and Yip, W and Maiorano, BA and Tateo, V and Spiess, PE and Pal, SK and Necchi, A},
title = {Impact of Age on Outcomes in Metastatic Non-Clear Cell Renal Cell Carcinoma: A Real-World TriNetX Analysis From the Global Society of Rare Genitourinary Tumors (GSRGT).},
journal = {Clinical genitourinary cancer},
volume = {24},
number = {8},
pages = {102658},
doi = {10.1016/j.clgc.2026.102658},
pmid = {42777623},
issn = {1938-0682},
abstract = {BACKGROUND: Malignancies arising in young adults often exhibit biological and clinical behaviors distinct from those in older patients. Limited data exist on the prognostic impact of age in metastatic non-clear cell renal cell carcinoma (mnccRCC). This study compared survival outcomes by age using the large-scale TriNetX database.

METHODS: We performed a retrospective analysis of mnccRCC patients receiving ≥1 line of therapy across TriNetX-participating institutions. Patients were stratified by age (<45 vs. ≥45 years). Kaplan-Meier analysis estimated progression-free survival (PFS) and overall survival (OS). Propensity score matching (PSM) adjusted for sex, race, histological subtype, metastasis sites, cytoreductive nephrectomy, and treatment type (immune checkpoint inhibitors [ICI]-containing vs. non-ICI regimens).

RESULTS: Among 758 patients with mnccRCC, 382 received first-line therapy during the study period (2015-2025) and were included in the analysis. 257 had papillary histology, 23 chromophobe, 18 collecting duct, 60 unclassified, and 24 other rare entities. Median age was 62.7 years; 69% male; 27% stage IV at diagnosis; 69% underwent radical nephrectomy. First-line regimens included ICI monotherapy (24.9%), tyrosine kinase inhibitors (TKI) monotherapy (53.9%), ICI + TKI (5%), and mTOR inhibitors (5.2%). Younger patients (<45, n = 54) had more liver, bone, lymph node, and brain metastases, whereas lung metastases were more frequent in older patients (P = .018). PFS was shorter in younger patients (14.9 vs. 30 months; P = .03), and OS showed a trend (17.7 vs. 36 months; P = .10). PSM analysis confirmed a PFS trend (14.6 vs. 36.5 months; P = .07), while OS differences were not significant (17.8 vs. 43.1 months; P = .12). In papillary mnccRCC, younger patients showed shorter PFS (20.4 vs. 26.9 months) and OS (22.5 vs. 33.3 months) with nonsignificant trends.

CONCLUSIONS: Younger mnccRCC patients (<45) presented with metastases at sites associated with poor prognosis and trends toward shorter PFS and OS, suggesting more aggressive disease biology. These findings support validation and consideration of tailored or more intensive strategies for younger patients.},
}

@article {pmid42777710,
year = {2026},
author = {Irajizad, E and Rudsari, HK and Gendarme, S and Vykoukal, J and Wu, R and Dennison, JB and Karimi, N and Darbaniyan, F and Moghaddam, SJ and Do, KA and Feng, Z and Ostrin, E and Hanash, S and Fahrmann, JF},
title = {A blood-based metabolic signature for earlier detection of lung cancer.},
journal = {Cell reports. Medicine},
volume = {},
number = {},
pages = {103059},
doi = {10.1016/j.xcrm.2026.103059},
pmid = {42777710},
issn = {2666-3791},
abstract = {Metabolomic profiling was applied to 1,259 sera collected within five years of a lung cancer diagnosis and 8,470 non-case sera from ever-smoker participants in the Prostate, Lung, Colorectal, and Ovarian (PLCO) Cancer Screening Trial to identify metabolic signatures for the earlier detection of lung cancer. We develop a panel of five lung cancer-associated metabolites (L5MetP: diacetylspermine, creatine riboside, arginine, hypoxanthine, and acylcarnitine C18:1) to assess 1-year risk of lung cancer. In the testing set, the L5MetP achieves an area under the receiver operating characteristic curve (AUC) of 0.79 (95% CI: 0.76-0.82) for 1-year risk of lung cancer. The L5MetP also complements existing clinical risk models that predict risk incident lung cancer as well as those that predict death from lung cancer. The L5MetP provides a means for identifying ever-smoker individuals who are lung cancer to inform on the need for lung cancer screening.},
}

@article {pmid42779338,
year = {2026},
author = {Mian, H and Faisal, MS and Chen, T and Brazauskas, R and Oloyede, T and Ahmed, N and Afrough, A and Anderson, LD and Banerjee, R and Berdeja, J and Bidikian, A and Devos, J and Dhakal, B and Dias, A and Dima, D and Efebera, YA and Gowda, L and Hansen, DK and Hashmi, H and Landau, HJ and Lekakis, L and Mirza, AS and Narra, R and Patel, K and Rosko, AE and Schroeder, M and Sidana, S and Usmani, S and Pasquini, MC and Nishihori, T and Akhtar, OS and Mohan, M},
title = {Efficacy and safety of frail patients treated with ciltacabtagene autoleucel in the real world: A Center for International Blood and Marrow Transplant Research analysis.},
journal = {Cancer},
volume = {132},
number = {19},
pages = {e70614},
pmid = {42779338},
issn = {1097-0142},
support = {27307C0011/ES/NIEHS NIH HHS/United States ; U01 AI184132/AI/NIAID NIH HHS/United States ; U24CA076518/CA/NCI NIH HHS/United States ; 27305C0011/ES/NIEHS NIH HHS/United States ; U24 CA076518/CA/NCI NIH HHS/United States ; U24CA076518/HL/NHLBI NIH HHS/United States ; 27398C0011/ES/NIEHS NIH HHS/United States ; U24CA076518//National Institute of Allergy and Infectious Diseases/ ; UG1 HL174426/HL/NHLBI NIH HHS/United States ; 75R60222C00011/HRSA/HRSA HHS/United States ; },
mesh = {Humans ; Female ; *Multiple Myeloma/therapy/mortality/drug therapy ; Male ; Aged ; *Frailty ; Middle Aged ; *Immunotherapy, Adoptive/methods/adverse effects ; Frail Elderly ; Treatment Outcome ; Progression-Free Survival ; Registries ; Receptors, Chimeric Antigen ; },
abstract = {BACKGROUND: Ciltacabtagene autoleucel (cilta-cel), an anti-B-cell maturation antigen (BCMA) chimeric antigen receptor T-cell (CAR-T) therapy, is approved for relapsed/refractory multiple myeloma (RRMM).

METHODS: Using the Center for International Blood and Marrow Transplant Research registry, this study evaluated outcomes of frail patients receiving commercial cilta-cel from March 2022 to December 2023. Frailty was defined by an adapted simplified score incorporating age, performance status, and comorbidities.

RESULTS: Among 541 patients with available frailty status, 183 (33.8%) were frail and 358 (66.2%) were nonfrail. Overall response rates were comparable (frail 82.8% vs. nonfrail 88.5%). However, frail patients had inferior progression-free survival (PFS) (12-month PFS, 62.7% [95% confidence interval (CI), 53.6%-71.3%] vs. 75.9% [95% CI, 70.4%-81.1%]; p < .01) and overall survival (OS) (12-month OS 72.8% [95% CI, 64.9%-80.0%] vs. 90.4% [95% CI, 86.6%-93.7%]; p < .01). Twelve-month treatment-related mortality in frail patients was 6.8% (95% CI, 3.4%-11.2%) versus 3.6% (95% CI, 1.8%-6.1%), p = .12. Cytokine release syndrome (grade ≥2) occurred in 22.4% of frail versus 17.9% of nonfrail patients (p = .05), and immune effector cell-associated neurotoxicity (ICANS) of any grade was reported in 32.2% versus 17.6% (p < .01). Rates of cranial nerve palsies and Parkinsonism were comparable. Prolonged cytopenia (>day 30) was more common in frail patients (30.6% vs. 21.2%; p < .01). On multivariable analysis, frailty independently predicted worse PFS (hazard ratio [HR], 1.67; 95% CI, 1.16-2.40), OS (HR, 2.46; 95% CI, 1.57-3.87), and higher odds of any-grade ICANS (odds ratio, 2.01; 95% CI, 1.32-3.08) (all p < .01).

CONCLUSIONS: Cilta-cel remains effective in frail RRMM, but frailty is associated with reduced survival and increased toxicity, supporting tailored CAR-T strategies.},
}

Humans
Female
*Multiple Myeloma/therapy/mortality/drug therapy
Male
Aged
*Frailty
Middle Aged
*Immunotherapy, Adoptive/methods/adverse effects
Frail Elderly
Treatment Outcome
Progression-Free Survival
Registries
Receptors, Chimeric Antigen

@article {pmid42779343,
year = {2026},
author = {Meshinchi, S and Locatelli, F},
title = {Search for leukemia-restricted targets: a new paradigm for precision immunotherapy in acute myeloid leukemia.},
journal = {Haematologica},
volume = {},
number = {},
pages = {},
doi = {10.3324/haematol.2026.301517},
pmid = {42779343},
issn = {1592-8721},
abstract = {Acute myeloid leukemia (AML) remains a major therapeutic challenge despite remarkable advances in genomic characterization. Although molecular profiling has transformed disease classification and risk stratification, treatment for most patients continues to rely on cytotoxic chemotherapy regimens developed more than 50 years ago. Numerous attempts to improve outcomes through treatment intensification, alternative chemotherapy approaches, and targeted agents have produced incremental benefits for selected patient populations, but have failed to fundamentally alter outcomes for many high-risk AML subtypes. A major obstacle to the broader application of immunotherapy in AML has been the absence of targets that clearly distinguish leukemic cells from normal hematopoietic tissues. Consequently, most immune-based therapies have focused on AML-associated antigens such as CD33, CD123, and CLEC12A, resulting in a narrow therapeutic window and significant hematopoietic toxicity. Recent advances in large-scale transcriptomic profiling, integrated genomic analyses, and immunopeptidomics have enabled systematic identification of AML-restricted biomarkers linked to leukemia-defining oncogenic programs. Rather than seeking a universal AML antigen, these approaches have uncovered subtype-specific targets, including FOLR1 in CBFA2T3::GLIS2 AML, CLEC2A in KMT2A-rearranged AML, mesothelin or CD7 in selected high-risk AML subsets, and intracellular targets such as WT1, PRAME, NPM1 neoantigens, and fusion-derived peptides. These discoveries have created opportunities for immunotherapeutic approaches capable of selectively targeting leukemic cells, while preserving normal hematopoiesis. This Spotlight Review discusses the evolution of AML biomarker discovery from prognostic classification to therapeutic target identification and highlights emerging AML-restricted biomarkers that may enable a new generation of biologically-precise immunotherapies for molecularly defined AML subsets.},
}

@article {pmid42779880,
year = {2026},
author = {Dadabhai, S and Samandari, T and Zhang, B and Hudson, A and Mkhize, NN and Tapley, A and Andriesen, J and Moore, PL and Chirenje, Z and Elyanu, PJ and Makhema, J and Kamuti, E and Nuwagaba-Biribonwoha, H and Kee, JJ and Hu, J and Baloyi-Oseh, K and Shah, P and Khuto, K and Miner, MD and Lessells, R and Bhebhe, S and Hermanus, T and Kaldine, H and Takalani, A and Yacovone, M and Polakowski, L and Hural, J and Fisher, LH and Margaret, CA and Aweyo, F and Badal-Faesen, S and Brumskine, WL and Coetzer, S and Dawson, R and Delany-Moretlwe, S and Gill, KM and Hosseinipour, MC and Innes, S and Kassim, P and Kafulafula, EG and Laher, F and Mandona, NM and Malahleha, M and Malulike, VL and Mathebula, M and Mboya, G and Mitha, E and Mngadi, K and Mda, P and Moloantoa, T and Naicker, N and Naicker, V and Nanvubya, A and Nchabeleng, M and Otieno, W and Potgieter, EL and Potloane, D and Punt, Z and Said, JA and Singh, Y and Tayob, MS and Wabwire, DO and Cohen, MS and McElrath, MJ and Andersen-Nissen, E and Ferrari, G and Kublin, JG and Bekker, LG and Gilbert, PB and Mgodi, NM and Kotze, PL and Huang, Y and Garrett, N and Gray, GE and Corey, L},
title = {Relative efficacy, safety and immunogenicity of bivalent versus monovalent COVID-19 mRNA booster vaccines: a randomized trial.},
journal = {Research square},
volume = {},
number = {},
pages = {},
pmid = {42779880},
issn = {2693-5015},
support = {T32 AI007044/AI/NIAID NIH HHS/United States ; UM1 AI068614/AI/NIAID NIH HHS/United States ; UM1 AI068618/AI/NIAID NIH HHS/United States ; UM1 AI068635/AI/NIAID NIH HHS/United States ; UM1 AI068619/AI/NIAID NIH HHS/United States ; },
abstract = {The relative efficacy, safety, and immunogenicity of monovalent mRNA-1273 (ancestral WA1) versus bivalent mRNA-1273.222 (ancestral plus omicron BA.4/BA.5) boosting have not been studied prospectively where HIV and SARS-CoV-2 seroprevalence are high. CoVPN 3008 (NCT05168813) was a randomized, double-blinded trial in seven African countries during omicron waves, enrolling people with HIV (PWH) or comorbidities associated with severe COVID-19 who had previously received mRNA-1273. Participants were randomized 1:1 to intramuscular monovalent or bivalent booster and routinely PCR-tested for SARS-CoV-2. Between 10/2022 and 03/2023, 3,988 participants (3,086 PWH) received bivalent (n=2012) or monovalent (n=1976) booster. By month 12, 293 COVID-19 cases and 221 asymptomatic infections occurred, including one severe case. COVID-19 rates did not differ between arms (hazard ratio [HR] 0.92, 95% CI 0.73-1.15, P=0.45). Combined COVID-19 and asymptomatic infection was 15% lower with the bivalent (239 vs. 275; HR 0.85, 0.71-1.01, P=0.07), and asymptomatic infection alone was 24% lower (HR 0.76, 0.59-1.00, P=0.05). Neutralizing antibody titers to BA.4/5 and XBB.1.5, measured in 100 PWH per arm, boosted higher in bivalent recipients (P=0.026 and 0.002). Adverse events were similar. In predominantly PWH, the bivalent booster was well tolerated, elicited superior immunogenicity against omicron variants, and appeared to protect against asymptomatic infection but not COVID-19.},
}

@article {pmid42779881,
year = {2026},
author = {Kikawa, C and Butler, A and Huddleston, J and Turner, SA and Peck, H and Englund, JA and Lacombe, K and Busch, M and Lanteri, MC and Stone, M and Spencer, B and Greninger, AL and Smith, DJ and Wallace, S and Marshall, HS and Tosif, S and Hensley, SE and Barr, IG and Bloom, JD},
title = {Near real-time data on the human neutralizing antibody landscape to influenza virus in summer of 2026 shows antigenic advance of H3N2 subclade K region D mutants and H1N1 D.3.1.1 Sa mutants.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
pmid = {42779881},
issn = {2692-8205},
abstract = {Human seasonal influenza evolves rapidly, necessitating twice yearly decisions about whether to update the strains in the vaccine. To help inform this decision, we have been using high-throughput sequencing-based neutralization assays to make twice yearly measurements of how recent human sera neutralize current human H3N2 and H1N1 strains. Here we provide the third installment in this series of measurements by reporting 52,268 titers representing neutralization of 148 viral strains by 355 human sera collected between April and August of 2026. Our measurements show that new H3N2 subclade K strains with mutations in antigenic region D and new H1N1 subclade D.3.1.1 strains with mutations in antigenic region Sa (such as G155E) have reduced neutralization by human sera, with notable heterogeneity in the impact of some of these mutations across sera from different individuals. This paper is accompanied by an interactive summary (https://jbloomlab.github.io/flu-seqneut-2026/summary.html) that enables detailed exploration of the results, and all titer data are publicly available for further analysis to aid vaccine antigen selection and studies of viral evolution.},
}

@article {pmid42779973,
year = {2026},
author = {Sims, JN and Gen, R and Sprouse, K and Park, YJ and Wang, Z and Amaya, M and Jays, A and Larsen, BB and Stewart, C and Brown, JT and Ragotte, R and Ravichandran, R and Ruth, G and Li, X and Vafeados, D and Bloom, JD and Broder, C and Veesler, D and Baker, D},
title = {Computational design of potent, broadly neutralizing anti-Nipah virus and Hendra virus miniproteins.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
pmid = {42779973},
issn = {2692-8205},
support = {DP1 AI158186/AI/NIAID NIH HHS/United States ; U19 AI181930/AI/NIAID NIH HHS/United States ; U19 AI142764/AI/NIAID NIH HHS/United States ; 75N93022C00036/OD/NIH HHS/United States ; U19 AI181881/AI/NIAID NIH HHS/United States ; },
abstract = {The prototype members of the genus Henipavirus, Nipah virus (NiV) and Hendra virus (HeV), cause recurrent zoonotic spillovers with case fatality rates ranging from 40-90% in humans. Currently, there are no approved vaccines or therapeutics for use in humans. Neutralizing antibodies targeting the NiV/HeV F- or G-glycoproteins protect animals from lethal challenge and are a main correlate of protection. However, antibody-based formulations are expensive, typically requiring hospital admission for administration and cold-chain for storage and transportation. To address the lack of shelf-stable clinical countermeasures, we computationally designed thermostable miniproteins that cross-react with subnanomolar affinities with both NiV and HeV F and G glycoproteins and inhibit viral entry in vitro with potencies comparable to lead antibodies. Oligomerized forms of these miniproteins have enhanced potency relative to their monomeric building blocks and increase the barrier for emergence of escape mutants, establishing them as promising preclinical candidates against these deadly viruses.},
}

@article {pmid42754228,
year = {2026},
author = {Gagelmann, N and Salit, RB and Schroeder, T and Chiusolo, P and Finazzi, MC and Gurnari, C and Pagliuca, S and Rautenberg, C and Rubio, MT and Maciejewski, JP and Vannucchi, A and Guglielmelli, P and Nozzoli, C and Leimkühler, N and Angelucci, E and Gambella, M and Rambaldi, A and Reinhardt, HC and Bacigalupo, A and Scott, BL and Heidel, FH and Popat, U and Kröger, N},
title = {iMTSS: an integrated framework for biology- and patient-driven prognosis in myelofibrosis undergoing transplantation.},
journal = {Transplantation and cellular therapy},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.jtct.2026.09.029},
pmid = {42754228},
issn = {2666-6367},
abstract = {BACKGROUND: Allogeneic hematopoietic cell transplantation is the only curative treatment for myelofibrosis, but failure occurs by two mechanistically distinct routes: relapse of the neoplasm, which reflects its underlying genetics, and non-relapse mortality, which reflects whether the patient and graft tolerate the procedure. Established prognostic systems either lack molecular granularity or were derived in the non-transplant setting, and all collapse these two routes into a single survival estimate. None can indicate why an individual patient is at risk, or which class of intervention might reduce that risk.

OBJECTIVE: To determine why an individual patient is at risk and to develop and validate an integrated framework that quantifies biology- and patient-driven prognosis.

STUDY DESIGN: We analyzed 1,550 adults undergoing first allogeneic transplantation for primary or secondary myelofibrosis across international centers, the largest genomically annotated transplant cohort in this disease. The cohort was split into development (n=930) and validation (n=620) sets. Overall survival was modeled by Cox regression; relapse and non-relapse mortality were modeled as competing events by Fine-Gray subdistribution-hazard regression at 2 years. Discrimination was assessed by the concordance index with bootstrap confidence intervals. The molecular contribution was quantified by variance decomposition of, and robustness to the analytic choices was examined by resampling.

RESULTS: A genetically defined disease-intrinsic axis, including TP53 allelic state, RAS pathway mutations, ASXL1 and driver genotype, blasts and blood counts, predicted 2 year relapse incidence (validation concordance 0.69, 95% CI 0.63 to 0.74), whereas a non-overlapping host and structural axis, including portal vein thrombosis, donor type, patients' performance status, and age predicted 2-year non-relapse mortality (0.63, 95% CI 0.59 to 0.68). The two scores shared only 3.4% of their variance, indicating that a patient's disease genetics carried almost no information about non-relapse mortality. Variance decomposition showed that TP53 allelic state alone accounted for 30% of the relapse score. Recombined, the framework discriminated overall survival (concordance 0.640, 95% CI 0.616 to 0.662) better than every established prognostic system. For proof of concept, 3 risk groups separated in the validation cohort, with 5 year survival of 72%, 58%, and 39% (P<0.001), and the models were well calibrated.

CONCLUSIONS: Relapse and non-relapse mortality after transplantation for myelofibrosis are governed by distinct dimensions. Estimating both outcomes independently with genetic and clinical information, in addition to overall survival, establishes an individualized basis for transplant decision-making. The calculator is openly available (https://imtss-calculator.com).},
}

@article {pmid42755219,
year = {2026},
author = {Raman, G and Vivek, M and Hasan, R and Keel, S and Connelly-Smith, L},
title = {Breakthrough Hemolysis in Paroxysmal Nocturnal Hemoglobinuria: Mechanistic Insights and Management Strategies.},
journal = {Transfusion},
volume = {},
number = {},
pages = {},
doi = {10.1111/trf.70379},
pmid = {42755219},
issn = {1537-2995},
abstract = {BACKGROUND: Paroxysmal nocturnal hemoglobinuria (PNH) is a clonal hematopoietic stem cell disorder caused by somatic mutations in the PIGA gene, resulting in loss of glycosylphosphatidylinositol (GPI)-anchored proteins, including the complement regulatory proteins, CD55 and CD59. Their absence leads to complement-mediated intravascular hemolysis. Patients may present with anemia, hemoglobinuria, renal injury, and potentially life-threatening thromboses. Complement inhibitors have transformed treatment for PNH. Terminal complement inhibitors reduce intravascular hemolysis and transfusion requirements but do not prevent C3-mediated extravascular hemolysis. Proximal complement inhibitors address both intravascular and extravascular hemolysis, but some are associated with a higher risk of breakthrough hemolysis (BTH). This article describes a transfusion-independent PNH patient on pegcetacoplan who developed severe BTH post-HLA desensitization using therapeutic plasma exchange (PLE) prior to hematopoietic cell transplantation.

METHODS: The authors reflect on several potential contributors including iatrogenic removal of pegcetacoplan, TPE, IVIG, and ABO-mismatched platelets, offering guidance on reducing the risk of BTH and potential management strategies.

RESULTS: The authors provide a detailed description of the patient case, discussing bio-, pharmacologic-, and transfusion-related factors which may promote BTH in PNH patients.

CONCLUSION: This article provides the authors' assessments highlighting the complexity of BTH in PNH patients receiving complement inhibitors, particularly in the setting of TPE and transfusion. Evaluation should consider potential precipitants of BTH, including iatrogenic drug removal and complement-amplifying conditions such as transfusions. Adjunctive C5 inhibition may be required in acute settings, and further studies are needed to define optimal dosing strategies.},
}

@article {pmid42755783,
year = {2026},
author = {Arzoumanian, A and Markarian, S and Johnson, A and Mastro, E and Jil-Agopian, S and Duggan, C and Hovhannisyan, M and Louis, H and Shekherdimian, S},
title = {Gap analysis of breast cancer care at tertiary facilities in Armenia.},
journal = {Frontiers in oncology},
volume = {16},
number = {},
pages = {1907028},
pmid = {42755783},
issn = {2234-943X},
abstract = {Breast cancer is the leading cause of cancer mortality among women globally. Armenia has one of the highest breast cancer mortality rates in the world, with an age standardized mortality-to-incidence ratio of 0.41, indicating that two in five breast cancer patients die from the disease. The factors contributing to this disproportionate mortality burden are poorly understood. The present study utilized a validated survey across four high-capacity cancer facilities to produce a national gap analysis of breast cancer care in Armenia. We find that the tertiary facilities surveyed broadly possess the fundamental technological and personnel resources required for modern breast cancer care; however, it is apparent that challenges exist with early detection, timely diagnosis, and successful treatment. Based on these findings, policy considerations could prioritize breast cancer mortality reduction through early detection, establishment of a cancer registry, streamlining cancer care, and reducing the financial burden of care on patients.},
}

@article {pmid42757810,
year = {2026},
author = {Guorgui, JG and Childers, CP},
title = {Trends in Medicare Work Relative Value Unit Payment Rates Across Physician Specialties: 2018-2024.},
journal = {Journal of the American College of Surgeons},
volume = {},
number = {},
pages = {},
doi = {10.1097/XCS.0000000000002202},
pmid = {42757810},
issn = {1879-1190},
abstract = {BACKGROUND: Recent Medicare Physician Fee Schedule revisions have sought to narrow perceived compensation differences between medical and surgical specialties, but their effects on work relative value unit (wRVU) payment rates are unknown. We estimated contemporary specialty-level wRVU payment rates and trends from 2018 through 2024.

STUDY DESIGN: Repeated cross-sectional analysis of Medicare Part B fee-for-service claims linked CMS Physician Time File, Addendum B, and Physician/Supplier Procedure Summary Master File data at the CPT-specialty-year level across 42 specialties (27 medical, 15 surgical). The primary outcome was annual specialty-level wRVU payment rate (wRVUs/min). Linear regression quantified trajectories. A counterfactual holding service times at 2018 values estimated rates assuming constant service times.

RESULTS: The medical-surgical payment-rate gap narrowed from 5.4% in 2018 (0.0405 vs 0.0426 wRVUs/min; P=.051) to 1.6% in 2024 (0.0428 vs 0.0435; P=.26), with convergence concentrated in 2021 and 2023, coinciding with evaluation and management revaluations. Primary care (+1.7%/year; P=.009) and nonsurgical nonprocedural specialties (+1.8%/year; P=.006) increased faster than surgical specialties (+0.4%/year). Under the counterfactual, 2024 rates exceeded actual values by 8.9% for primary care, 6.9% for nonsurgical nonprocedural, 5.0% for nonsurgical procedural, 4.5% for surgical, and 0.1% for facility-based specialties, narrowing the medical-surgical gap to 0.8%.

CONCLUSIONS: From 2018 through 2024, the Medicare medical-surgical wRVU payment-rate gap narrowed from 5.4% to 1.6% under current CMS valuation assumptions. These findings suggest the Medicare Physician Fee Schedule may be a limited instrument for narrowing broader specialty compensation differences.},
}

@article {pmid42758055,
year = {2026},
author = {Duarte, C and Bosma, GN and Abbott, D and Jean-Louis, G and Kabat, M and Stapor, D and Hill, B and Musoke, N and Gorzewski, AM and Selvakumar, T and Trabolsi, A and Greenberg, MR and Hansen, A and Bailey, N and Shadman, M and Kendall, E and Ahmed, N and Lutfi, F and Johnson, PC and Di, M and Patel, K and Bock, AM and Rhodes, JM and Schatz, JH and Hess, B and Karmali, R and Frosch, ZAK and Ip, A and Cherng, HJ and Jasem, J and Bair, S and Haverkos, B and Kamdar, M and Major, A},
title = {TP53-Altered Aggressive Large B-Cell Lymphoma (LBCL) Outcomes by Treatment Modality: A Multicenter Cohort From 14 US Centers.},
journal = {European journal of haematology},
volume = {},
number = {},
pages = {},
doi = {10.1111/ejh.70330},
pmid = {42758055},
issn = {1600-0609},
support = {P30 CA240139/CA/NCI NIH HHS/United States ; UM1 TR004399//NIH/NCATS Colorado CTSA/ ; },
abstract = {Advances in the treatment of large B-cell lymphoma (LBCL) have expanded therapeutic options beyond conventional chemoimmunotherapy to include cellular and targeted therapies. There is growing interest in identifying subsets of LBCL that may benefit from these novel approaches based on histopathologic and molecular features. Molecular subclassification has identified an LBCL A53 phenotype characterized by TP53 alterations, a subgroup historically associated with poor outcomes following standard therapy. To better define progression-free and overall survival outcomes in TP53-altered LBCL in the contemporary treatment era, we conducted a multicenter cohort study evaluating responses to first-, second-, and third-line therapies. Our findings demonstrate that TP53-altered LBCL can be cured with first-line curative intent chemoimmunotherapy. In the second and third-line setting, outcomes did not significantly differ between different treatment approaches, though improved PFS was seen with CAR-T in the second line for double hit patients. This study represents the largest reported cohort of patients with TP53-altered LBCL and provides important insights into treatment outcomes across lines of therapy in the era of novel agents.},
}

@article {pmid42760475,
year = {2026},
author = {Yi, JC and Ballard, S and Artim, EJ and Walsh, C and Baker, KS},
title = {A mixed methods study of adolescent and young adult cancer survivors and their utilization of a survivorship clinic: Barriers and facilitators.},
journal = {Journal of cancer survivorship : research and practice},
volume = {},
number = {},
pages = {},
pmid = {42760475},
issn = {1932-2267},
abstract = {PURPOSE: The National Standards for Cancer Survivorship Care propose health system policies to develop survivorship programs. Little is known about the utilization, barriers, and facilitators of survivorship care amongst adolescent and young adult (AYA: ages 15-39 at diagnosis) cancer survivors.

METHODS: Participants included AYAs who were 1-5 years post-treatment and eligible to participate in a parent study testing a digital health intervention. The electronic health record (EHR) was queried to determine who had been seen in the Survivorship Clinic, and qualitative interviews were conducted with a randomly selected subset of those participants.

RESULTS: Of 836 survivors eligible for the parent trial, only 38 (4.5%) were seen in the Survivorship Clinic (86.8% female, 71.1% White, 86.8% not Hispanic, 65.7% breast cancer). A subset enrolled in the parent trial (n = 147) was screened for approach for qualitative interviews. Forty interviews were completed (mean age = 38.4 (SD = 4.4), 50% breast cancer, 78% female, 83% White, 83% Non-Hispanic White, 92% college or more education) with only one seen in the Survivorship Clinic. Participants identified barriers including lack of awareness, avoidance, and lack of time. Referrals from care teams, information about services provided, and telehealth were identified as factors that would have facilitated them seeking survivorship care.

CONCLUSIONS: Few AYAs sought survivorship services that could assist them in addressing the late effects of their cancer diagnosis and treatment.

Lack of awareness of the survivorship clinic was the most significant barrier, and a referral from their oncology care team would have facilitated them scheduling a visit.},
}

@article {pmid42763656,
year = {2026},
author = {Shepherd, A},
title = {Is it time to complete the transition from Masaoka-Koga to TNM in thymic tumors?-the con perspective.},
journal = {Mediastinum (Hong Kong, China)},
volume = {10},
number = {},
pages = {45},
pmid = {42763656},
issn = {2522-6711},
}

@article {pmid42765319,
year = {2026},
author = {Ezzat, D and Pabon, MA and Li, L and Chang, A and De Moor, N and Yu, Z and Cho, SMJ and Natarajan, P and Spracklen, CN and LeBlanc, ES and Eaton, CB and LaMonte, MJ and Stefanick, ML and Manson, JE and Parikh, N and Reiner, AP and Roh, JD and Soria-Contreras, DC and Hoshi, RA and Mora, S and Demler, OV and Powe, CE and Honigberg, MC},
title = {Hypertensive Disorders of Pregnancy and Cardiovascular-Kidney-Metabolic Syndrome.},
journal = {Hypertension (Dallas, Tex. : 1979)},
volume = {},
number = {},
pages = {},
pmid = {42765319},
issn = {1524-4563},
support = {75N92021D00002/HL/NHLBI NIH HHS/United States ; 25SFRNCCKMS1443062/AHA/American Heart Association-American Stroke Association/United States ; 25SFRNPCKMS1463898/AHA/American Heart Association-American Stroke Association/United States ; 75N92021D00001/HL/NHLBI NIH HHS/United States ; 75N92021D00003/WH/WHI NIH HHS/United States ; K24 HL136852/HL/NHLBI NIH HHS/United States ; 24RGRSG1275749/AHA/American Heart Association-American Stroke Association/United States ; 75N92021D00004/WH/WHI NIH HHS/United States ; R01 HL181150/HL/NHLBI NIH HHS/United States ; R01 HL170058/HL/NHLBI NIH HHS/United States ; 75N92021D00005/WH/WHI NIH HHS/United States ; K99 HL177340/HL/NHLBI NIH HHS/United States ; },
abstract = {BACKGROUND: Hypertensive disorders of pregnancy (HDP) affect over 10% of pregnancies worldwide, but their association with cardiovascular-kidney-metabolic (CKM) syndrome remains unexplored.

METHODS: The present study included parous UK Biobank participants. The primary exposure was HDP history. CKM syndrome was categorized from stage 0 (no risk factors) to 4 (cardiovascular disease). Logistic regression tested the association of HDP history with CKM stage, adjusted for age, age[2], race, Townsend Deprivation Index, and smoking status. Cox models evaluated progression to stage 4, in addition, adjusting for baseline CKM stage. Replication analyses were performed in the Women Health Initiative, with CKM stage assessed at 2 study visits.

RESULTS: Among 219 639 UK Biobank (mean age, 56.9 years) and 3591 Women Health Initiative participants (61.7 years at baseline, 78.1 years at the follow-up visit), 2836 (1.3%) and 304 (8.4%), respectively, had a history of HDP. In the UK Biobank, HDP history was significantly associated with higher CKM stage (adjusted odds ratio, 3.40 [95% CI, 3.12-3.71]; P<0.001) in ordinal logistic regression. Compared with CKM stage 0, HDP history was associated with higher odds of stages 2 to 4 (adjusted odds ratios, 6.34, 11.20, and 7.43, respectively; all P<0.001). Over a median follow-up of 13.6 years, prior HDP was associated with progression to stage 4 (adjusted hazard ratio, 1.24 [95% CI, 1.10-1.40]; P<0.001). Replication in the Women Health Initiative produced consistent results.

CONCLUSIONS: HDP history was associated with greater CKM stage and progression to advanced CKM syndrome, supporting its use as an early life predictor of adverse CKM trajectories.},
}

@article {pmid42766303,
year = {2026},
author = {Disis, ML and Chun, BMN and Dhillon, KK and Liao, JB and Hunter, N and Cecil, DL},
title = {Vaccines for Cancer: A Translational Science Review.},
journal = {JAMA},
volume = {},
number = {},
pages = {},
doi = {10.1001/jama.2026.15540},
pmid = {42766303},
issn = {1538-3598},
abstract = {IMPORTANCE: Advances in tumor immunology and vaccine technology are reshaping cancer vaccine development after decades of limited clinical success. More than 2000 immunogenic tumor proteins or antigens have been identified, the types of immune responses required for tumor eradication have been defined, and safe and effective vaccine delivery technologies have been developed. This progress has renewed clinical investigation of cancer vaccines for multiple types of cancer.

OBSERVATIONS: Vaccines, such as those against human papillomavirus and hepatitis B, are composed of (1) an antigen target, (2) an adjuvant to activate the immune system, and (3) a vaccine delivery vehicle. Antigens can be derived from tumor mutations termed neoantigens, or cancer-associated nonmutated proteins, which are normal human proteins that are abnormally expressed in cancer. The tumor can also act as an antigen source, such as when immunization occurs with whole tumor cells or by directly injecting an immunogenic substance into the tumor to elicit an adaptive immune response. T and B lymphocytes, cells of the adaptive immune system, are stimulated by cancer vaccines and can provide a highly specific and durable immune response directed against cancer. Vaccines that elicit adaptive immunity are approved for cancer treatment. Sipuleucel-T, a vaccine against the antigen prostatic acid phosphatase, reduced all-cause mortality compared with placebo in men with metastatic castrate-resistant prostate cancer (32% vs 23%; hazard ratio, 0.78 [95% CI, 0.61-0.98]; P = .03). Compared with granulocyte-macrophage colony-stimulating factor, a systemic immune stimulant, talimogene laherparepvec increased rates of a 6-month or longer complete or partial response, defined as the disappearance of all treated disease and at least a 50% decrease in the sum of the products of perpendicular diameters of the measurable lesion with no new lesions, respectively, when injected into advanced melanoma lesions (16.3% [95% CI, 12.1%-20.5%] vs 2.1% [95% CI, 0%-4.5%]; odds ratio, 8.9; P < .001). Most cancer vaccines have mild adverse effects, such as fatigue, fever, and injection site reactions. Combining cancer vaccines with chemotherapy or immunotherapy can increase the magnitude of the immune response and potentially result in greater reduction in cancer size. Combining the personalized mutation-based messenger RNA (mRNA) vaccine (mRNA-4157) with the immune checkpoint inhibitor pembrolizumab for resected high-risk stage IIIB to IV cutaneous melanoma improved relapse-free survival compared with pembrolizumab alone (76.6% vs 60%; hazard ratio, 0.56 [95% CI, 0.31-1.02]; P = .05). Cancer vaccines are undergoing evaluation in clinical trials to prevent cancer recurrence and for primary cancer prevention.

CONCLUSIONS AND RELEVANCE: Cancer vaccines can treat several types of malignant neoplasms, including melanoma, prostate cancer, and bladder cancer. Adverse effects associated with cancer vaccines are generally mild and of short duration, promoting eventual integration of vaccination into treatment regimens with chemotherapy and immunotherapy. Cancer vaccines are increasingly undergoing evaluation for primary prevention.},
}

@article {pmid42766795,
year = {2026},
author = {Chow, EJ and Lee, ED and Hershberger, M and Jenssen, K and Di, C and Doody, DR and Hogue, B and Mendoza, JA and Muller, TM and Schenk, JM and Syrjala, KL and Xu, Y and Yi, J and Zhao, YQ and Armstrong, GT and Neuhouser, ML and Oeffinger, KC},
title = {Correction: Protocol for a Sequential Multiple Assignment Randomized Trial to Improve Physical Activity and Diet Quality in Survivors of Cancer.},
journal = {JMIR research protocols},
volume = {15},
number = {},
pages = {e111094},
pmid = {42766795},
issn = {1929-0748},
support = {U24 CA055727/CA/NCI NIH HHS/United States ; P30 CA015704/CA/NCI NIH HHS/United States ; R01 CA263144/CA/NCI NIH HHS/United States ; P30 CA021765/CA/NCI NIH HHS/United States ; P30 DK035816/DK/NIDDK NIH HHS/United States ; },
}

@article {pmid42769245,
year = {2026},
author = {Kang, DW and Patel, D and Field, CJ and Boulé, NG and Fairey, AS and Schadler, KL and Courneya, KS},
title = {Changes in circulating immune cells and cytokines after high-intensity aerobic exercise in patients with prostate cancer undergoing active surveillance from the ERASE randomized controlled trial.},
journal = {Frontiers in immunology},
volume = {17},
number = {},
pages = {1923463},
pmid = {42769245},
issn = {1664-3224},
mesh = {Humans ; Male ; *Prostatic Neoplasms/immunology/blood/therapy ; *Cytokines/blood/immunology ; Aged ; Middle Aged ; *High-Intensity Interval Training ; Killer Cells, Natural/immunology ; *Exercise ; },
abstract = {BACKGROUND: Exercise can modulate immune function and inflammatory signaling in cancer populations; however, its effects on the immune system in men with localized prostate cancer undergoing active surveillance are unknown. This study examined the effects of high-intensity interval training (HIIT) on circulating immune cell phenotypes, function, and systemic cytokine levels in this clinical setting.

METHODS: This was a secondary analysis of the Exercise During Active Surveillance for Prostate Cancer (ERASE) trial, a single-center randomized controlled trial. Fifty-two men with localized prostate cancer on active surveillance were randomized to a 12-week supervised aerobic HIIT program (n=26) or usual care (n=26). HIIT consisted of three sessions per week at 85% to 95% of peak oxygen consumption. Fasting blood samples were collected at baseline and post-intervention. Changes in immune cell subsets (T cells, B cells, and NK cells; flow cytometry), NK cell cytotoxicity, and plasma cytokine concentrations were assessed. Analyses of covariance were used to compare between-group differences.

RESULTS: The HIIT group attended 96% of prescribed sessions. Compared with usual care, the HIIT group showed a significant increase in the proportion of the circulating major NK-cell subset (CD3-CD56+CD16+) (adjusted between-group difference, 2.0%; 95% CI, 0.3 to 3.7; p=0.024) and PBMC-mediated cytotoxicity against K562 (2.9%; 95% CI, 0.3 to 5.4; p=0.031). A significant between-group decrease was also observed in basophil counts (-0.04 ×10[9]/L; 95% CI, -0.07 to -0.01; p = 0.011), with no differences in other leukocyte populations. HIIT significantly reduced plasma levels of IL-4 (-0.02 pg/mL; 95% CI, -0.03 to -0.01; p = 0.011) and IL-12p70 (-0.14 pg/mL; 95% CI, -0.23 to -0.06; p = 0.002) compared with usual care. No significant between-group differences were observed in T cell or B cell subsets, or other inflammatory cytokines including IL-6 and TNF-α.

CONCLUSIONS: A 12-week supervised HIIT program significantly increased the proportion of the circulating major NK-cell subset and PBMC-mediated cytotoxicity while reducing IL-4 and IL-12p70 concentrations in men with prostate cancer undergoing active surveillance. Because these were peripheral-blood measures rather than tumor-level readouts, and given the exploratory design and number of comparisons, these findings should be interpreted as hypothesis-generating and require confirmation in larger, adequately powered studies.},
}

Humans
Male
*Prostatic Neoplasms/immunology/blood/therapy
*Cytokines/blood/immunology
Aged
Middle Aged
*High-Intensity Interval Training
Killer Cells, Natural/immunology
*Exercise

@article {pmid42770214,
year = {2026},
author = {Mayer, KH and Kotze, P and Lombaard, J and Caraco, Y and Peer, A and Poovan, N and Khalsa, S and Khetan, S and Shapiro, AE and Rassool, M and Gonzalez, A and Singh, Y and Sinclair, G and Riddler, SA and Buchbinder, S and Ben-Ami, E and Turner, M and Vesay, M and Homony, B and Evans, B and Grandhi, A and Zhang, C and Robertson, MN and Kapoor, Y and Matthews, RP and Plank, RM},
title = {Alimatravir Oral Once Monthly in Adults With Low Likelihood of HIV Exposure: A Randomized, Double-Blind, Placebo-Controlled Study.},
journal = {The Journal of infectious diseases},
volume = {},
number = {},
pages = {},
doi = {10.1093/infdis/jiag439},
pmid = {42770214},
issn = {1537-6613},
support = {//MSD/ ; },
abstract = {BACKGROUND: Long-acting oral options for human immunodeficiency virus-1 (HIV-1) pre-exposure prophylaxis are needed to address challenges with adherence to once-daily regimens. Alimatravir is an oral nucleoside reverse transcriptase translocation inhibitor with pharmacokinetic properties supporting once-monthly dosing.

METHODS: In this double-blind, placebo-controlled study, adults aged 18-65 years with low likelihood of HIV-1 exposure were randomly assigned 2:2:2:1 to receive 6 oral doses of alimatravir (3, 6, or 12 mg) or placebo once every 4 weeks. The primary outcome was the proportion of participants with adverse events through 8 weeks after the last dose, assessed in participants who received at least one dose of study intervention. Additional outcomes were the pharmacokinetics of alimatravir in plasma (all participants) and alimatravir-triphosphate in peripheral blood mononuclear cells (∼ 20 participants from each alimatravir dose group).

RESULTS: Three hundred fifty participants were included in the analyses (median age 28 years; 58% female): 301 received alimatravir 3 mg (n = 101), 6 mg (n = 101), or 12 mg (n = 99) and 49 received placebo. Adverse event rates were comparable for alimatravir 3 mg (61.4% [62/101]), 6 mg (68.3% [69/101]), 12 mg (66.7% [66/99]), and placebo (63.3% [31/49]). Study intervention was discontinued because of an adverse event in 1.0% (3/301) of participants who received alimatravir and 4.1% (2/49) who received placebo. Pharmacokinetic parameters for alimatravir and alimatravir-triphosphate were dose-proportional and support a once-monthly dosing interval.

CONCLUSIONS: The favorable safety, tolerability, and pharmacokinetics of alimatravir and alimatravir-triphosphate support continued development of alimatravir as oral monthly pre-exposure prophylaxis.

CLINICAL TRIALS REGISTRATION: ClinicalTrials.gov Identifier NCT06045507; https://www.clinicaltrials.gov/search.},
}

@article {pmid42749807,
year = {2026},
author = {Itagi, P and Schuster, SL and Arora, S and Persse, TW and Waters, JA and Yang, M and Min, A and Chandra, P and Adil, M and Galipeau, PC and Rudoy, D and Kreitman, AS and Lin, Y and Ko, M and Sayar, E and Patton, RD and Kollath, L and Meis, A and Lindergren, S and Ji, N and Ali, K and Venkatesh, H and Wladyka, CL and McDeed, AP and Mills, CB and Vashisth, M and Kim, JY and Nadal, R and Hawley, JE and Yezefski, TA and Psutka, SP and Gore, JL and Lin, DW and Nelson, PS and Cheng, HH and Schweizer, MT and Fong, L and Lee, JK and Yu, EY and Corey, E and Morrissey, C and Grivas, P and Montgomery, RB and Wright, JL and Haffner, MC and Vakar-Lopez, F and Mian, OY and Lam, HM and Hsieh, AC and Ha, G},
title = {Evolution and heterogeneity of lethal metastatic bladder cancer subtypes.},
journal = {Nature},
volume = {},
number = {},
pages = {},
pmid = {42749807},
issn = {1476-4687},
abstract = {Histological variation is a prognostic feature of metastatic urothelial cancer[1-3], but its evolutionary trajectory remains poorly defined. We developed a metastatic bladder cancer rapid autopsy programme enriched in histological subtypes[4] to profile individuals with terminal disease. Here by reconstructing the evolutionary histories of patient tumours, we show that metastasis-to-metastasis seeding is the dominant pattern of cancer spread and that increased polyclonal migration predicts poor prognosis. The burden, heterogeneity and timing of genomic alterations differ markedly among histological subtypes. Plasmacytoid and neuroendocrine variants develop early driver alterations associated with shorter survival. Mutational signature analyses and experimental models demonstrated that plasmacytoid tumours uniquely use the Fanconi anaemia pathway to mitigate chemotherapy-induced genomic scarring. Single-nucleus profiling revealed mixed cell states in histological subtypes and an association between transcriptional heterogeneity and patient survival. Characterization of the tumour microenvironment uncovered distinct immune states across subtypes, with plasmacytoid tumours exhibiting immune-inflamed profiles, whereas squamous tumours are predominantly immunosuppressive. Last, we demonstrate that post-mortem cell-free DNA captures genomic and transcriptional heterogeneity of the subtypes, which provides a potential strategy for noninvasive assessment of tumour identity and aggressiveness. Our results provide new insights into how tumour heterogeneity shapes the evolutionary history of disease progression in bladder cancer histological subtypes.},
}

@article {pmid42749856,
year = {2026},
author = {Pichardo, MS and Aragaki, AK and Manson, JE and Pan, K and Jung, SY and Rohan, TE and Mszar, R and Chlebowski, RT},
title = {Menopausal hormone therapy and primary liver cancer: long-term follow-up of the women's health initiative randomized trials.},
journal = {British journal of cancer},
volume = {},
number = {},
pages = {},
pmid = {42749856},
issn = {1532-1827},
support = {75N92021D00002/HL/NHLBI NIH HHS/United States ; 75N92021D00005/WH/WHI NIH HHS/United States ; LRP0000062905//U.S. Department of Health & Human Services | NIH | National Cancer Institute (NCI)/ ; 75N92021D00001/HL/NHLBI NIH HHS/United States ; 75N92021D00003/WH/WHI NIH HHS/United States ; L32 CA305494/CA/NCI NIH HHS/United States ; 75N92021D00004/WH/WHI NIH HHS/United States ; },
abstract = {BACKGROUND: Long-term results on liver cancer incidence and mortality are reported from two Women's Health Initiative randomized trials evaluating menopausal hormone therapy.

METHODS: 16,608 postmenopausal women with a uterus were randomized to conjugated equine estrogen (CEE) 0.625 mg/d plus medroxyprogesterone acetate (MPA) 2.5 mg/d or placebo and 10,739 women with hysterectomy were randomized to 0.625 mg/d of CEE-alone or placebo.

RESULTS: After nearly 24 years follow-up and 74 incident liver cancers, neither CEE-alone nor CEE plus MPA influenced liver cancer development (CEE-alone vs placebo (11 vs 15 cancers; hazard ratio [HR] 0.75; 95% CI, 0.34-1.63; CEE plus MPA vs placebo (30 vs 18 cancers; HR 1.63; 95% CI, 0.91-2.92). CEE plus MPA did not significantly influence liver cancer mortality: 27 vs 22 deaths (HR 1.18; 95% CI, 0.67-2.07). In subgroup analyses, CEE plus MPA vs placebo was associated with more liver cancers among women aged 50-59 years (10 vs 0 cancers (P-trend 0.01) and prior oral contraceptive users (HR 4.30, 95% CI, 1.46-12.72; P-interaction 0.01).

CONCLUSIONS: These findings indicate no overall influence of menopausal hormone therapy on liver cancer incidence or mortality although a possible increased risk with CEE plus MPA in select subgroups warrants further investigation.

TRIAL REGISTRATION: clinicaltrials.gov Identifier: NCT00000611.},
}

@article {pmid42751311,
year = {2026},
author = {Kotton, CN and Workowski, KA and Kumar, PN and Avery, RK and Chemaly, RF and Issa, NC and Ramgopal, M and Schiffer, JT and Albrecht, J and O'Neal, HR and Chandrasekar, P and Schreibman, TS and Ramesh, M and Ison, MG and Sumner, ME and Dane, A and Surujbally, B and Timmler, B and Rangaraju, M and Papanicolaou, GA and Birkmann, A and Wald, A},
title = {Efficacy and Safety of Pritelivir vs Foscarnet for the Treatment of Acyclovir-Refractory Herpes Simplex Virus Infection in Immunocompromised Adults: A Randomized, Open-Label Phase 2 Trial.},
journal = {Open forum infectious diseases},
volume = {13},
number = {9},
pages = {ofag539},
pmid = {42751311},
issn = {2328-8957},
abstract = {BACKGROUND: Immunocompromised patients are at risk for severe, prolonged herpes simplex virus (HSV) recurrences. Refractory disease and intolerance to standard therapy drive an unmet medical need. Pritelivir, a novel HSV helicase-primase inhibitor, has shown favorable tolerability and efficacy in immunocompetent adults.

METHODS: PRIOH-1, a multicenter, randomized, open-label Phase 2 trial, compared oral pritelivir (400-mg loading dose followed by 100 mg daily) with intravenous foscarnet (40 mg/kg q8h or 60 mg/kg q12h) for up to 28 days in immunocompromised adults with acyclovir-refractory HSV (Part A). Participants with refractoriness/intolerance to foscarnet received pritelivir (Part B). The primary end point was time to lesion healing; secondary end points included healing rate, HSV DNA detection, and resistance.

RESULTS: Twenty-two participants enrolled in Part A, 8 in Part B. In Part A, median time to healing was 26.0 days (95% CI, 13.0-31.0) with pritelivir, vs not estimable (95% CI, 20.0-NE) with foscarnet (HR, 2.7; 95% CI, 0.33-21.8; P = .34). Investigator-assessed healing rates were 93% with pritelivir and 57% with foscarnet, a 36.2% difference (95% CI, -10.1 to 74.1; P = .077). Postbaseline HSV DNA detection rates were 34.8% and 50.0%, respectively (P = .42). Treatment-emergent adverse events occurred in 60% of pritelivir- and 100% of foscarnet-treated participants; serious treatment-emergent adverse events were less frequent with pritelivir. In Part B, the median time to healing was 19.0 days, with a 63% healing rate.

CONCLUSIONS: Pritelivir demonstrated encouraging efficacy and favorable safety in immunocompromised adults with limited treatment options, supporting Phase 3 evaluation for the treatment of refractory HSV infection in this population.},
}

@article {pmid42752878,
year = {2026},
author = {Watling, CZ and Petrick, JL and Graubard, BI and Hong, HG and Zhang, X and Barnett, MJ and Barnard, ME and Chen, Y and Heather Eliassen, A and Gaziano, JM and Huang, WY and Kang, JH and Koshiol, J and Lee, IM and Loftfield, E and Moore, SC and Mucci, LA and Neuhouser, ML and Newton, CC and Sesso, HD and Shrubsole, M and Sinha, R and Tinker, L and Triplette, M and Um, CY and Visvanathan, K and Wactawski-Wende, J and Watts, EL and Willett, WC and Wu, F and Zheng, W and Campbell, PT and Hofmann, JN and Purdue, MP and Barupal, D and McGlynn, KA},
title = {Per- and polyfluoroalkyl substances levels other than PFOS, PFOA, or PFHxS and liver cancer risk: a nested case-control analysis.},
journal = {Journal of the National Cancer Institute},
volume = {},
number = {},
pages = {},
doi = {10.1093/jnci/djag325},
pmid = {42752878},
issn = {1460-2105},
abstract = {Epidemiologic studies of PFAS and liver cancer risk have produced conflicting results with no strong or clear associations for pre-diagnostic perfluorooctanesulfonate (PFOS), perfluorooctanoate (PFOA), and perfluorohexanesulfonate (PFHxS). We now report analyses of nine additional PFAS in a nested case-control study within 12 prospective cohorts (853 cases, 853 matched controls) in the United States. Using multivariable-adjusted conditional logistic regression, we estimated odds ratios per 90th vs. 10th percentile increase in PFAS levels. Perfluoroheptanoic acid (PFHpA) was positively associated with liver cancer risk (OR: 1.78, 95% CI: 1.26-2.52); no associations were observed for other PFAS. Significant heterogeneity was observed by sex, cancer subtype, and time from blood collection. Associations were stronger among males (OR: 3.72, 95% CI: 2.10-6.59), for hepatocellular carcinoma (4.53, 2.59-7.94), and for those diagnosed ≤10 years after blood collection (3.17, 1.80-5.57). Given continued use of short-chain PFAS in consumer products, further research on their effects on liver health is warranted.},
}

@article {pmid42753317,
year = {2026},
author = {Valadez-Cosmes, P and Maitz, K and Lagler, A and Kindler, O and Mujkanovic, NC and Raftopoulou, S and Kienzl, M and Juvan, ZN and Santiso, A and Brcic, L and Gorkiewicz, G and Lindenmann, J and Sattler, W and Heinemann, A and Schicho, R and Marsche, G and Houghton, AM and Kargl, J},
title = {Myeloperoxidase promotes a tumorigenic microenvironment in non-small cell lung cancer.},
journal = {Redox biology},
volume = {97},
number = {},
pages = {104399},
pmid = {42753317},
issn = {2213-2317},
abstract = {Myeloperoxidase (MPO) is a heme peroxidase that is mainly expressed and secreted by neutrophils. MPO's role in inflammatory diseases has been highlighted in recent years, but its role in tumor development remains unclear. Therefore, we investigated the role of MPO in non-small cell lung cancer (NSCLC). In silico analysis revealed a survival benefit in patients with NSCLC and low MPO expression. Furthermore, a syngeneic tumor model using MPO knockout (KO) mice revealed that mice lacking MPO had lower tumor growth than controls. The reduction in tumor size was accompanied by an increase in lymphoid populations, including natural killer cells and CD8[+] T cells, suggesting a shift to a more anti-tumorigenic immune environment in MPO-KO mouse tumors. The T cell induced interferon-gamma (IFN-γ) expression was increased in MPO-KO tumors, indicating increased tumoricidal activity. CD8 depletion abolished the previously observed reduction in tumor size in MPO-KO mice, indicating that CD8[+] T cells play an important role. In vitro, T cells treated with MPO showed reduced proliferation and IFN-γ expression. Furthermore, MPO associated directly with T cells. Interestingly, MPO[+] lymphocytes, including CD8[+] T cells, were found in tumor samples from patients with NSCLC. Our findings suggest that MPO plays an immunosuppressive role in NSCLC.},
}

@article {pmid42753723,
year = {2026},
author = {Tignor, NL and Koptyra, M and Chowdhury, S and Petralia, F and Gritsenko, MA and Ma, W and Zhu, Y and Marino, GB and Song, X and Migliozzi, S and Whiteaker, JR and Rykunov, D and Hu, Y and Hosseini, N and Rokita, JL and da Veiga Leprevost, F and Rathi, KS and Chen, L and Wang, YT and Weitz, KK and Chu, RK and Moore, RJ and Krek, A and Fu, W and Wang, X and Deng, EZ and Tsai, CF and Sagendorf, T and Petyuk, VA and Shi, T and Fillmore, TL and Zhao, R and Monroe, ME and Dannappel, MV and Daniel, P and Zhao, L and Ivey, RG and Voytovich, UJ and Yaron-Barir, TM and Huntsman, EM and Johnson, JL and Abedin, N and Li, YC and Santi, M and Dupal, D and Lilly, J and Kraya, A and Dybas, JM and Zhang, B and Zhong, C and Brown, MA and Phul, S and Wafula, E and Farrel, A and Geng, Z and Corbett, RJ and Naqvi, AS and Miller, DP and Mason, J and Patton, TS and McGrory, S and Robins, S and Heath, A and Sullivan, C and Coleman, N and Morgan, A and Garofano, L and Reva, B and Schadt, EE and Smith, RD and Mesri, M and Robles, AI and Cantley, LC and Ding, L and Rodland, KD and Zhang, B and Nesvizhskii, AI and Iavarone, A and Cieslik, M and Ippolito, JE and Storm, PB and Rubin, JB and Firestein, R and Ma'ayan, A and Zhang, H and Paulovich, AG and Liu, T and Resnick, A and Rood, BR and Wang, P and , and , and , },
title = {Proteogenomic analysis of pediatric and AYA high-grade glioma reveals age-dependent biology, female-male differences, and kinase targets.},
journal = {Cell reports. Medicine},
volume = {},
number = {},
pages = {103024},
doi = {10.1016/j.xcrm.2026.103024},
pmid = {42753723},
issn = {2666-3791},
abstract = {High-grade gliomas (HGGs) in children and adolescents and young adults (AYA) exhibit distinct biology across the neurodevelopmental spectrum. To dissect tumor-intrinsic molecular characteristics independent of developmental variation, we perform comprehensive proteogenomic analyses of tumors from 112 HGG patients aged 0-40 years. Our multi-omics analysis identifies two AYA subgroups-adolescents (aged 15-26 years) and young adults (aged 26-40 years)-with distinct molecular profiles and survival outcomes. Tumor-normal comparisons and survival modeling highlight roles of oxidative phosphorylation and neuronal system biology in glioma progression. Causal network analysis and cell line studies provide a rationale for personalized therapies targeting candidate kinases, such as CDK8. Survival modeling, clustering, and immune-landscape analyses identify proteins, post-translational modifications, and immune signatures linked to outcomes and reveal clinically relevant differences between male and female patients.},
}

@article {pmid42749798,
year = {2026},
author = {Simonich, CAL and McMahon, TE and Juviler, G and Kampman, L and Chu, HY and Bloom, JD},
title = {Mutational constraints on RSV F and its neutralization by antibodies.},
journal = {Nature},
volume = {},
number = {},
pages = {},
pmid = {42749798},
issn = {1476-4687},
support = {P30 CA015704/CA/NCI NIH HHS/United States ; U19 AI181767/AI/NIAID NIH HHS/United States ; K12 HD000850/HD/NICHD NIH HHS/United States ; T32 HD007233/HD/NICHD NIH HHS/United States ; R01 AI141707/AI/NIAID NIH HHS/United States ; },
abstract = {New antibodies targeting the F protein of respiratory syncytial virus (RSV) have substantially reduced infant hospitalizations[1]. However, viral resistance is a concern: one antibody failed clinical trials because of a resistant strain[2], and sporadic resistance mutations to the most widely used antibody (nirsevimab) have been identified[3-6]. Here we define how RSV F mutations affect antibody neutralization. We first provide a biophysical model of how the buffering of bivalent IgG binding combines with the lower Fab potency of nirsevimab to subtype B to make resistance to this antibody more common in subtype B than A strains. We then perform pseudovirus deep mutational scanning to safely measure how nearly all mutations to F affect its cell entry function and neutralization by IgG and Fab forms of nirsevimab, clesrovimab and several other key antibodies. We use these measurements to enable real-time surveillance of RSV sequences for antibody resistance, and show that resistant strains have arisen sporadically but are at present rare. Overall, our work shows how Fab potency and epitope specificity combine to determine how viral mutations affect antibody neutralization, enables monitoring for natural RSV strains resistant to antibodies of public-health importance, and can help guide development of future antibodies with resilience to viral escape.},
}

@article {pmid42747695,
year = {2026},
author = {Stock, W and Cassaday, RD and DeAngelo, DJ and Advani, A and Gokbuget, N and Ribera, J and Jiang, W and Pulido, S and Vandendries, E and Braniff, N and Jabbour, E and Kantarjian, H},
title = {Outcomes by Body Mass Index in Patients With B-Cell Precursor Acute Lymphoblastic Leukemia Treated with Inotuzumab Ozogamicin.},
journal = {Targeted oncology},
volume = {},
number = {},
pages = {},
pmid = {42747695},
issn = {1776-260X},
abstract = {BACKGROUND: Inotuzumab ozogamicin (lnO) is approved for the treatment of adults with relapsed/refractory B-cell precursor acute lymphoblastic leukemia. Elevated body mass index (BMI) could be associated with worse outcomes.

OBJECTIVE: To conduct post hoc BMI-stratified efficacy/safety analyses of lnO.

PATIENTS AND METHODS: Pooled data from phase 1-4 InO trials were analyzed, with patients grouped by BMI: < 25 kg/m[2] (normal), 25-30 kg/m[2] (overweight), and > 30 kg/m[2] (obese), including a subset of morbidly obese (> 40 kg/m[2]) patients. Descriptive analyses included efficacy, safety, and pharmacokinetic simulations for InO.

RESULTS: Across 338 patients, complete remission (CR) or CR with incomplete count recovery (CRi) was achieved in 69.7%, 75.9%, 68.7%, and 84.6% patients in the < 25, 25-30, > 30, and > 40 kg/m[2] subgroups, respectively. The 24-month probability of progression-free survival was 19.9%, 12.8%, 10.9%, and 23.1%; the 24-month overall survival probability was 28.1%, 22.1%, 17.5%, and 23.1% in these subgroups, respectively. Most deaths were due to progressive disease. Most patients experienced treatment-emergent adverse events (TEAEs), with similar incidence across subgroups. The most common grade ≥ 3 TEAE was neutropenia (36.1%), with sinusoidal obstruction syndrome (SOS) observed in 8.3%. 143 patients (42%) proceeded to hematopoietic stem cell transplant (HSCT) after lnO treatment, with 31 (21.7%) experiencing post-HSCT SOS; the BMI > 40 kg/m[2] subgroup (n = 7 receiving HSCT) had the numerically highest post-HSCT non-relapse mortality. In simulations for dose capping (capped maximum dose), exposure metrics were similar across subgroups with/without dose capping.

CONCLUSION: Efficacy/safety outcomes with InO were consistent across BMI subgroups. Dose-capping does not appear to be required.},
}

@article {pmid42748045,
year = {2026},
author = {Gogebakan, KC and Lange, J and Gulati, R and Etzioni, R},
title = {Expected late-stage reduction under extended screening in the first multicancer screening trial.},
journal = {Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology},
volume = {},
number = {},
pages = {},
doi = {10.1158/1055-9965.EPI-26-0942},
pmid = {42748045},
issn = {1538-7755},
abstract = {The first multi-cancer screening trial did not meet its primary endpoint of reducing late-stage (stage III/IV) incidence after three screening rounds. We used a previously developed multi-cancer natural history model to assess whether continued annual screening could have produced larger benefit. The model was calibrated to match observed late-stage reductions by screening round and aggregate episode sensitivity for the trial's 12 prespecified cancers, then used to project late-stage reductions over 10 annual screening rounds. Among the 15 best-calibrated models, early-stage preclinical detectable period ranged from 0.46 to 1.36 years, and per-cancer early-stage sensitivities from 30%-60% of previously reported sensitivities for clinically diagnosed cancers. The calibrated models reproduced the excess late-stage incidence in round 1 and increasing reductions thereafter. With continued screening, late-stage reductions by screening round plateaued at 13%-17% (range across 15 models), while cumulative late-stage reduction reached 9%-13% by round 10.},
}

@article {pmid42749377,
year = {2026},
author = {Samur, S and Hoban, O and Gu, NY and Carter, GC and Palomares, M and Arrick, B and Gursel, E and Yildiz, Y and Ayer, T and Chhatwal, J and Parsons, HA},
title = {Recurrence detection in patients with triple-negative breast cancer following the current standard of care: a microsimulation model.},
journal = {BMJ open},
volume = {16},
number = {9},
pages = {e115240},
pmid = {42749377},
issn = {2044-6055},
mesh = {Humans ; Female ; *Triple Negative Breast Neoplasms/diagnosis/pathology/mortality/therapy ; *Neoplasm Recurrence, Local/diagnosis ; Middle Aged ; *Standard of Care ; Neoplasm Staging ; Disease-Free Survival ; Computer Simulation ; },
abstract = {OBJECTIVES: Breast cancer is the most common cancer among women in the USA, accounting for approximately 31% of new cases and 15% of cancer-related deaths in females. Triple-negative breast cancer (TNBC) is the most lethal subtype with 29 months median overall survival. Despite curative-intent surgery and systemic adjuvant therapy, many patients remain at risk for recurrence. We developed a comprehensive model for patients with operable stage II and III TNBC, adhering to the current standard-of-care clinical follow-up recommendations, to evaluate the effectiveness of these recommendations in detecting recurrence among patients with newly diagnosed TNBC.

DESIGN: An individual-level state transition (microsimulation) model was built with a lifetime horizon using monthly cycles. The model integrated treatment and surveillance recommendations per current guidelines.

SETTING: The currently recommended treatment and surveillance modalities by the National Comprehensive Cancer Network guidelines for surveilling patients with TNBC after diagnosis.

PARTICIPANTS: Female patients aged 49 years who were newly diagnosed with operable stage II or III TNBC.

OUTCOME MEASURES: Cumulative recurrences, detected recurrences, detection rate, overall survival and recurrence-free survival in a 5-year horizon, as well as average life expectancy, were the outcome measures used.

RESULTS: Our model estimated a 5-year overall survival rate of 81.4%±0.1% (SE) for patients with stage II or III TNBC, with a recurrence-free survival rate of 78.3%±0.1% (SE). Over the same period, 7.4%±0.1% (SE) of patients with TNBC were projected to experience recurrences (68% distant recurrence, 32% locoregional recurrence), with a detection rate of only 59.3%±0.2% (SE) among these recurrences. Our model estimated that 399 mammograms would be required to detect one locoregional recurrence and 279 other imaging tests would be needed to identify one distant recurrence.

CONCLUSIONS: Our clinically validated model sheds light on the outcomes for patients with TNBC, revealing the limitations in recurrence detection rates associated with current guidelines. These findings underscore the need for improved strategies during the surveillance period. As novel testing methods become available, this model can be instrumental in exploring how these innovations may improve patient outcomes.},
}

Humans
Female
*Triple Negative Breast Neoplasms/diagnosis/pathology/mortality/therapy
*Neoplasm Recurrence, Local/diagnosis
Middle Aged
*Standard of Care
Neoplasm Staging
Disease-Free Survival
Computer Simulation

@article {pmid42740607,
year = {2026},
author = {Lee, J and Minot, S and Dey, N},
title = {Pangenome analysis reveals both niche-specific "specialists" and microbial "side hustlers" in colorectal cancer microbiomes.},
journal = {Gut microbes},
volume = {18},
number = {1},
pages = {2728331},
pmid = {42740607},
issn = {1949-0984},
support = {U54 CA274374/CA/NCI NIH HHS/United States ; },
mesh = {*Colorectal Neoplasms/microbiology ; Humans ; Phylogeny ; *Bacteria/classification/genetics/isolation & purification ; *Gastrointestinal Microbiome/genetics ; },
abstract = {The gut microbiome is reproducibly implicated in colorectal cancer (CRC), yet the inter-study and interpersonal variability of certain species associations suggests that CRC microbiomes may be defined by convergent functional states achievable by phylogenetically diverse organisms. Distinguishing lineage-conserved "specialists" from taxonomically diverse "side hustlers"-organisms whose shared functional traits are dispersed across phylogenetically distant lineages-offers complementary translational insights: "specialists" are primary candidates for lineage-targeted biomarkers and inhibitors, while the shared functional architecture of "side hustlers" may reveal high-priority potential therapeutic targets robust to inter-individual variability. Here, we quantify phylogenetic coherence (monophyly) of 3,711 co-associated gene bins (CAGs) across 13 bacterial species and evaluate CRC associations across three independent cohorts, identifying hundreds of CAGs associated with CRC or health across a spectrum of monophyly scores, indicating that both states harbor a mixture of "specialist" and "side hustler" gene content. Strikingly, in Faecalibacterium prausnitzii-a species with a complex relationship to CRC-health-associated CAGs exhibited significantly higher monophyly scores than CRC-associated CAGs, consistent with health-linked traits being lineage-conserved while CRC-linked traits behave as polyphyletically distributed, potentially mobile "side hustlers." Across multiple CRC-associated species, we observe functional convergence in gene bins encoding Type IV secretion systems (T4SS), TonB-dependent receptors, and RagB/SusD nutrient uptake proteins. Fusobacterium animalis strains encode T4SS elements across bins with variable phylogenetic origins, representing simultaneous "specialist" and "side hustler" strategies within a single species. Pairwise interaction analysis further reveals synergistic interspecies associations, including co-occurrence of F. animalis and Clostridium scindens gene bins associated with a CRC probability of > 90%, suggesting that microbial "side hustlers" may amplify oncogenic risk through ecological interactions invisible to species-level analysis. These findings provide proof-of-principle that an ecological and evolutionary lens on the CRC microbiome can identify shared functional vulnerabilities and lineage-specific targets for microbiome-based cancer prevention.},
}

*Colorectal Neoplasms/microbiology
Humans
Phylogeny
*Bacteria/classification/genetics/isolation & purification
*Gastrointestinal Microbiome/genetics

@article {pmid42740668,
year = {2026},
author = {Gao, F and Dasgupta, S and Pasalar, S and Wang, Q and Alfaro, R and Pinto-Santini, D and Torres, TS and Sanchez, J and Lama, JR and Veloso, VG and Juraska, M and Cabello, R and Alarcon, JO and Grinsztejn, B and Caceres, CF and Rooney, JF and Duerr, A},
title = {Comparing Approaches for Estimating Counterfactual HIV Incidence Among Populations With High Vulnerability to HIV in Lima, Peru: A Multi-Study Comparative Analysis.},
journal = {Journal of the International AIDS Society},
volume = {29},
number = {9},
pages = {e70204},
pmid = {42740668},
issn = {1758-2652},
mesh = {Humans ; Peru/epidemiology ; Male ; *HIV Infections/epidemiology/prevention & control ; Incidence ; *Pre-Exposure Prophylaxis ; Adult ; Female ; Homosexuality, Male ; Young Adult ; Transgender Persons ; Prospective Studies ; },
abstract = {INTRODUCTION: The availability of highly efficacious HIV pre-exposure prophylaxis (PrEP) makes it unethical or infeasible to conduct inactive/placebo-controlled trials to evaluate new HIV prevention options. As a result, randomized active-control non-inferiority trials are typically employed; however, they require large sample sizes and extended follow-up. Moreover, their results can be hard to interpret. An alternative approach compares HIV incidence among individuals receiving a new PrEP product to a counterfactual incidence estimate-an estimate of what the HIV incidence would have been in the absence of PrEP.

METHODS: We leveraged data from three studies (AMP, Sabes and ImPrEP seroincidence) conducted among men who have sex with men and transgender persons in Lima, Peru, between 2013 and 2022 to estimate the counterfactual HIV incidence for two target populations represented by a clinical trial (AMP) and a non-interventional cohort study (Sabes). We evaluated three estimation methods: prospective cohort follow-up, recency testing and rectal gonorrhoea (RG) approaches. These approaches were compared directly using data from the same study, and we further assessed population adjustment approaches by comparing estimates across studies.

RESULTS: All three methods produced consistent HIV incidence estimates when applied to data collected from the same study. ​However, estimates differed when data from external studies were used, even after propensity score (PS) adjustment. For example, estimates for the AMP population using Sabes or ImPrEP data remained higher than the AMP gold-standard estimate. In contrast, adjusted estimates for the Sabes population using AMP or ImPrEP data were lower than the Sabes follow-up estimate. These differences underscore the challenges of applying external data and highlight the role of unmeasured population heterogeneity.

CONCLUSIONS: Counterfactual HIV incidence estimates can support evaluation of new PrEP agents when direct placebo comparisons are not possible. Estimates from recency-testing and RG approaches are promising when prospective follow-up is infeasible, but their validity depends on data quality and population similarity. PS methods improve comparability across populations but cannot fully account for unobserved differences. Triangulating across methods and sources can improve confidence in counterfactual estimates, which should be interpreted with careful attention to population context.},
}

Humans
Peru/epidemiology
Male
*HIV Infections/epidemiology/prevention & control
Incidence
*Pre-Exposure Prophylaxis
Adult
Female
Homosexuality, Male
Young Adult
Transgender Persons
Prospective Studies

@article {pmid42742049,
year = {2026},
author = {Smibert, OC and Kong, G and Markey, KA and Judd, LM and Howden, B and Stinear, TP and Gordon, C and Sharma, VJ and D'Costa, R and Sinclair, M and Majumdar, A and Starkey, G and Testro, A and Trubiano, JA and Slavin, MA and Kwong, JC},
title = {Donor Microbiota Features Associated With Liver Transplant Recipient Infectious Complications: A Pilot Study Using Deep Intestinal Sampling During Liver Procurement.},
journal = {Transplant infectious disease : an official journal of the Transplantation Society},
volume = {},
number = {},
pages = {e70322},
doi = {10.1111/tid.70322},
pmid = {42742049},
issn = {1399-3062},
support = {//National Health and Medical Research Council/ ; },
abstract = {BACKGROUND: The gut microbiota of living organ donors has been linked to transplant outcomes. However, little is known about the characteristics of the deceased donor gut microbiota or its potential impact on recipient outcomes.

METHODS: We analyzed the deep intestinal microbiota from 24 deceased donors. Samples included luminal stool from the right and left colon as well as bile. Microbial composition was characterized using 16S V4 rRNA sequencing. α- and β-diversity analyses were performed to compare microbial communities between donor enteric sites and against stool samples from 28 healthy community controls, 14 critically ill intensive care comparators, and 12 matched liver transplant recipients. Machine learning models and logistic regression analysis were applied to explore whether features of the donor microbiota could predict recipient post-transplant complications.

FINDINGS: The deceased donor microbiota showed an absence of the expected compositional variability between sampling sites, with no significant differences in either α- or β-diversity observed between bile, right and left colonic samples (all p > 0.05). Donor samples exhibited distinct microbial profiles compared with stool from both healthy and ICU comparators, including increased abundance of potential pathogens within the Enterobacteriaceae family (all p < 0.001). Features of the donor microbiota, particularly enrichment of Enterobacteriaceae, were associated with an increased risk of early post-transplant infection in recipients (≤ 30 days; p = 0.011).

INTERPRETATION: The deceased donor gut microbiota may represent a distinct microbial community with potential clinical relevance. Microbial profiling of donor enteric microbiota may help identify recipients at heightened risk of early post-transplant infectious complications.},
}

@article {pmid42742640,
year = {2026},
author = {Sehrawat, K and Polley, MC and Vogelbaum, MA and Gilbert, M and Chakravarti, A and Cahill, DP and Lassman, AB and Raleigh, DR and Sulman, EP and Machtay, M and Le, QT and Curran, W and Gondi, V and Mehta, MP},
title = {The evolution of RTOG and NRG Oncology CNS tumors clinical trials.},
journal = {Journal of neuro-oncology},
volume = {179},
number = {2},
pages = {},
pmid = {42742640},
issn = {1573-7373},
support = {U10 CA180822/CA/NCI NIH HHS/United States ; U10 CA180868/CA/NCI NIH HHS/United States ; UG1 CA189867/CA/NCI NIH HHS/United States ; U10CA180868 (NRG Oncology Operations), U10CA180822 (NRG Oncology SDMC), UG1CA189867 [National Cancer Institute Community Oncology Research Program (NCORP)] and Aurora NCORP Research Base grant (UG1CA189867)/NH/NIH HHS/United States ; },
mesh = {Humans ; *Central Nervous System Neoplasms/radiotherapy/therapy ; *Clinical Trials as Topic ; *Radiation Oncology ; },
abstract = {PURPOSE: Radiation Therapy Oncology Group (RTOG) and NRG Oncology have played a key role in shaping evidence-based management of central nervous system (CNS) tumors. These have defined standards for radiotherapy delivery, integrated systemic therapies for multimodal approaches, and advanced trial methodology across a range of CNS malignancies through large, multi-institutional studies. This is a comprehensive narrative review of trials involving adult CNS tumors, focused on gliomas, metastases, meningioma, and primary CNS lymphoma (PCNSL).

METHODS: Trials were identified through protocol archives, published literature, and curated trial inventories, and were analyzed with respect to treatment strategies, trial evolution, and impact on practice.

RESULTS: Early trials established foundational radiotherapy paradigms, including dose, volume, and fractionation standards. Subsequent studies demonstrated limitations of dose escalation and led to development of prognostic tools such as recursive partitioning analysis (RPA). In gliomas, these trials defined the role of chemoradiation, setting new standards of care (SOC), and clarified the limited benefit of treatment intensification, while recent studies explored molecularly selected therapies. In BM, randomized trials transformed management through stereotactic radiosurgery (SRS)-based approaches and hippocampal-avoidance whole brain radiotherapy (HA-WBRT), with incorporation of neurocognitive function (NCF) and quality-of-life (QOL) endpoints. Trials in meningioma provided some of the first prospective data supporting role of radiotherapy, and PCNSL trials established the superiority of chemoradiotherapy, and response-adapted deployment of WBRT.

CONCLUSION: RTOG and NRG Oncology trials have driven iterative, evidence-based advances in transitioning to precision. These efforts continue to inform contemporary guidelines and provide a framework for future trials integrating molecular stratification, advanced imaging, and novel therapeutic strategies.},
}

Humans
*Central Nervous System Neoplasms/radiotherapy/therapy
*Clinical Trials as Topic
*Radiation Oncology

@article {pmid42743457,
year = {2026},
author = {Gong, G and Roychoudhury, S and Meisner, A and Pusztai, L and Goldberg, SB and Wei, W},
title = {LEAD-ONC: A Platform for Reconstructing Survival Data From Trial Reports for Targeted Evidence Synthesis and Clinical Trial Design.},
journal = {JCO clinical cancer informatics},
volume = {10},
number = {3},
pages = {e2600099},
doi = {10.1200/CCI-26-00099},
pmid = {42743457},
issn = {2473-4276},
mesh = {Humans ; *Clinical Trials as Topic ; *Research Design ; Lung Neoplasms/mortality ; Carcinoma, Non-Small-Cell Lung/mortality ; Bayes Theorem ; Survival Analysis ; Kaplan-Meier Estimate ; },
abstract = {BACKGROUND AND SCOPE: Clinical trial design in oncology relies heavily on evidence synthesized from prior studies. However, relevant information, including Kaplan-Meier curves, baseline characteristics, and eligibility criteria, is typically embedded in figures, tables, and free text, making systematic extraction and quantitative synthesis challenging. We developed LEAD-ONC (Literature to Evidence for Analytics and Design in Oncology), a platform designed to transform published clinical trial reports into structured, analyzable data to support evidence-informed trial design.

SOLUTION: LEAD-ONC integrates large language models and computer vision techniques to extract multimodal information from published oncology trials, including survival curves, risk tables, and baseline characteristics. Individual patient data are reconstructed from digitized Kaplan-Meier curves, whereas baseline covariates are extracted and harmonized at the trial level across studies. The platform incorporates cross-trial similarity assessment to identify clinically comparable studies and applies Bayesian hierarchical survival modeling to generate predictive survival distributions for future trials.

EVALUATION: We demonstrate the utility of LEAD-ONC using a case study in metastatic non-small cell lung cancer. The platform successfully extracted and harmonized data from multiple phase III trials and generated predictive survival distributions for a target population defined by mixed histology. Model-based projections of median overall survival and treatment effect illustrate how the platform can support quantitative assumptions for trial design.

RELEVANCE: LEAD-ONC provides a scalable framework for systematic evidence synthesis from published literature. By enabling target population-specific survival projections, the platform supports more transparent and data-driven clinical trial design.

HOW TO ACCESS/USE: LEAD-ONC is available at: https://lead-onc.org/step1.},
}

Humans
*Clinical Trials as Topic
*Research Design
Lung Neoplasms/mortality
Carcinoma, Non-Small-Cell Lung/mortality
Bayes Theorem
Survival Analysis
Kaplan-Meier Estimate

@article {pmid42743551,
year = {2026},
author = {Parsons, HA},
title = {Can Biomarkers Effectively Guide Treatment Tailoring in Human Epidermal Growth Factor 2-Positive Early Breast Cancer?.},
journal = {Journal of clinical oncology : official journal of the American Society of Clinical Oncology},
volume = {},
number = {},
pages = {JCO2601857},
doi = {10.1200/JCO-26-01857},
pmid = {42743551},
issn = {1527-7755},
}

@article {pmid42745176,
year = {2026},
author = {Jacob-Dolan, C and Thomas, A and Reynolds, G},
title = {Immunity by Design: Engineering Pathogen-Specific Protection After Transplantation.},
journal = {Transplant infectious disease : an official journal of the Transplantation Society},
volume = {},
number = {},
pages = {e70320},
doi = {10.1111/tid.70320},
pmid = {42745176},
issn = {1399-3062},
}

@article {pmid42747321,
year = {2026},
author = {Zhang, S and Singh, O and Dazelle, K and Quezado, M and Cimino, PJ and Abdullaev, Z and Wu, J and Lucas, CH and Schreck, KC and Holdhoff, M and Pytel, P and Goodwill, V and Macaulay, R and McDonald, W and Seidman, R and Wood, M and Bharani, K and Neltner, J and Richard, H and Chang, K and Szymanski, L and Yip, S and Mukherjee, A and Lopes Abath Neto, O and Sharma, SJ and Green, R and Brown, D and Gubbiotti, MA and Ballester, LY and Eschbacher, J and Smith-Cohn, M and Gokden, M and Vincentelli, C and Yong, W and Lee, J and Mount, C and Fulmer, J and Sun, M and Ligon, K and Santi, M and Pai, EL and Yeaney, G and Alexandrescu, S and Raghavan, R and Fernandes, I and Reis, GF and Mandel, J and Caccamo, D and Rao, S and Butt, OH and Dahiya, S and Stone, S and Conway, K and Nasrallah, MP and Fuller, C and Toland, A and Lukas, RV and Cachia, D and Uhlmann, E and McCord, M and Helgager, J and Han, K and Perry, A and Perez, S and Daoud, E and BeDell, D and Highfield, H and Kobalka, P and Nix, JS and Nduom, E and Neill, S and Gilbert, M and Lakis, N and Fonseca, A and Shen, C and Yoda, R and Monterroza, L and Cohen, AL and Cathcart, S and Al Amin, MD and Campian, J and Aldape, K},
title = {High-grade astrocytoma with piloid features: a clinical and genomic analysis of prognostic factors using a large cohort.},
journal = {Neuro-oncology},
volume = {},
number = {},
pages = {},
doi = {10.1093/neuonc/noag145},
pmid = {42747321},
issn = {1523-5866},
abstract = {BACKGROUND: High-grade astrocytoma with piloid features (HGAP) is a recently defined tumor type that is not well-understood. Prognostic factors of clinical outcomes are not well-established.

METHODS: Methylation profiling was performed on tumor samples, many at the National Cancer Institute (NCI) Laboratory of Pathology, and others from publicly available sources. Methylation classifier scores of ≥ 0.90 to the HGAP class on the NCI-Bethesda classifier version 3 were included. Clinical features were collected from the medical record. Survival analyses were performed using the Kaplan-Meier and Cox-proportional hazards methods.

RESULTS: The cohort comprised 421 patients. There were high rates of ATRX alteration (62%), CDKN2A/B homozygous loss (78%) and MGMT promoter methylation (53%). MAPK alterations were identified in 74% of evaluable samples. The median age was 46 years, and posterior fossa location was predominant (52%). The median overall survival (OS) was 88 months. Older age (p = 0.01) and the presence of an ATRX alteration (p = 0.04) were found to be negative prognostic factors. The presence of cystic features on magnetic resonance imaging (MRI) was found to be favorably prognostic (p = 0.01). Factors that were not significantly associated with prognosis included histologic high-grade features, CDKN2A/B homozygous deletion, MGMT promoter methylation, extent of resection, and presence of NF1 syndrome.

CONCLUSIONS: This large cohort establishes relative frequencies of several important markers. Additionally, older age, the presence of an ATRX alteration, and cystic features on MRI were found to be prognostic. Our work may aid in optimizing treatment regimens for patients with this tumor type.},
}

@article {pmid42747330,
year = {2026},
author = {Zantek, ND and Alquist, CR and Hofmann, JC and Klingel, R and Levenbrown, Y and Onwuemene, OA and Patidar, G and Patriquin, CJ and Raval, JS and Sanchez, AP and Schneiderman, J and Tanhehco, YC and Connelly-Smith, L},
title = {Guidelines on the Use of Therapeutic Apheresis in Clinical Practice-Evidence-Based Approach From the Writing Committee of the American Society for Apheresis: The Tenth Special Issue.},
journal = {Journal of clinical apheresis},
volume = {41 Suppl 2},
number = {Suppl 2},
pages = {e70141},
pmid = {42747330},
issn = {1098-1101},
mesh = {Humans ; *Blood Component Removal/methods/standards ; *Evidence-Based Medicine ; United States ; Societies, Medical ; },
abstract = {The American Society for Apheresis (ASFA) Journal of Clinical Apheresis (JCA) Special Issue Writing Committee is charged with reviewing, updating, and categorizing indications for the evidence-based use of therapeutic apheresis (TA) in human disease. As in recent editions, the Tenth Edition of the JCA Special Issue committee has incorporated systematic review and evidence-based approaches in the grading of evidence and categorization of apheresis indications to make recommendations on the use of apheresis in a wide variety of diseases and conditions. This edition has largely maintained the general layout and concept of a fact sheet introduced in the Fourth Edition (2007). Each fact sheet succinctly summarizes the evidence for the use of TA in a specific disease entity or medical condition. The Tenth Edition comprises 93 fact sheets and 183 graded and categorized indications. This includes two new fact sheets and several changes to indications, categorization, or grade on existing fact sheets. The Tenth Edition of the JCA Special Issue seeks to continue to serve as a key resource that guides the utilization of TA in the treatment of human disease.},
}

Humans
*Blood Component Removal/methods/standards
*Evidence-Based Medicine
United States
Societies, Medical

@article {pmid42736534,
year = {2026},
author = {Aitken, SL and Aboujaoude, ER and Borjan, J and Tverdek, FP},
title = {Comparative Neurotoxicity of Polymyxin B and Colistin in Patients With Cancer.},
journal = {Pharmacotherapy},
volume = {46},
number = {10},
pages = {e70202},
pmid = {42736534},
issn = {1875-9114},
mesh = {Humans ; *Colistin/adverse effects/administration & dosage ; *Polymyxin B/adverse effects/administration & dosage ; *Anti-Bacterial Agents/adverse effects/administration & dosage ; Retrospective Studies ; *Neurotoxicity Syndromes/etiology/epidemiology ; Female ; Male ; *Neoplasms/complications/drug therapy ; Middle Aged ; Aged ; Gram-Negative Bacterial Infections/drug therapy ; Adult ; },
abstract = {BACKGROUND: The polymyxins, polymyxin B and colistin, are last-line options for the treatment of infections caused by drug-resistant gram-negative organisms. The comparative neurotoxicity of these agents using contemporary dosing is poorly understood. We sought to compare the incidence of neurotoxicity among recipients of polymyxin B or colistin.

METHODS: This was a single-center, retrospective cohort study of all patients who received colistin or polymyxin B for the treatment of a serious gram-negative infection between March 2016 and April 2020. The primary outcome of interest was treatment-emergent neurotoxicity, defined as new-onset perioral paresthesia, non-oral paresthesia, peripheral neuropathy, seizure, diaphragmatic paralysis, or other neurotoxicity. Bivariate analyses were performed using Fisher's exact test and the Wilcoxon rank-sum test; no multivariable analyses were performed.

RESULTS: A total of 82 patients receiving polymyxin B (n = 39) or colistin (n = 43) were identified. Neurotoxicity, nearly exclusively paresthesia, was more commonly seen in recipients of polymyxin B (10/39 evaluable patients, 26%) versus colistin (1/42 evaluable patients, 2%; p < 0.01). Neurotoxicity most commonly developed on the first day of therapy and resolved with discontinuation of therapy or prolongation of the infusion duration.

CONCLUSIONS: Polymyxin B is associated with significantly more neurotoxicity than colistin in unadjusted analyses. This potential risk should be considered when choosing between these two agents.},
}

Humans
*Colistin/adverse effects/administration & dosage
*Polymyxin B/adverse effects/administration & dosage
*Anti-Bacterial Agents/adverse effects/administration & dosage
Retrospective Studies
*Neurotoxicity Syndromes/etiology/epidemiology
Female
Male
*Neoplasms/complications/drug therapy
Middle Aged
Aged
Gram-Negative Bacterial Infections/drug therapy
Adult

@article {pmid42737570,
year = {2026},
author = {Hackmon, R and Geraghty, DE and Dunk, CE},
title = {Immunology of Normal Pregnancy and Preeclampsia and the Role of Placental Non-Classical HLA and Decidual NK Cells.},
journal = {International journal of molecular sciences},
volume = {27},
number = {17},
pages = {},
pmid = {42737570},
issn = {1422-0067},
mesh = {Humans ; Female ; Pregnancy ; *Pre-Eclampsia/immunology ; *Killer Cells, Natural/immunology ; *Decidua/immunology ; *Placenta/immunology/metabolism ; HLA-G Antigens/immunology ; *Histocompatibility Antigens Class I/immunology/metabolism ; *HLA Antigens/immunology ; Animals ; HLA-E Antigens ; },
abstract = {Pregnancy is considered a unique immunological process in which contact between the maternal innate immune system and the placental allograft results in maternal tolerance to paternally derived antigens. A growing body of research indicates that interactions between non-classical placental Human Leukocyte Antigen (NCHLA) and receptors on decidual Natural Killer (dNK) cells from early implantation are crucial to this process. Preeclampsia (PE), one of the leading causes of maternal and fetal morbidity and mortality, is also considered an autoimmune process. Currently, there is no treatment for PE except delivery. Most adverse outcomes derive from delayed diagnosis, while newer preventative therapies significantly improve outcomes. An early predictor of PE would enable universal screening, detect and treat high-risk populations earlier, and improve outcomes. Recently, we discovered that high placental HLA-E and G expression occurs during early normal pregnancies, and that placental NCHLA expression differs in PE. Others described the HLA-E/G complex, a potent immunosuppressor of dNK. Interestingly, dNK cells were found to have memory-like properties in binding to HLA-G and HLA-E. The theory proposed is that the HLA-G complex plays a major role in the etiology of PE. In this narrative review, we examine the relevant literature and present our recent findings and those of others that suggest a screening model for PE.},
}

Humans
Female
Pregnancy
*Pre-Eclampsia/immunology
*Killer Cells, Natural/immunology
*Decidua/immunology
*Placenta/immunology/metabolism
HLA-G Antigens/immunology
*Histocompatibility Antigens Class I/immunology/metabolism
*HLA Antigens/immunology
Animals
HLA-E Antigens

@article {pmid42728335,
year = {2026},
author = {Soares, RF and Chang, CH and Koerich, LB and Malik, HS and Kuhn, GCS},
title = {Retention of a single Cenp-C gene in different syntenic locations in the montium group of Drosophila species.},
journal = {Heredity},
volume = {},
number = {},
pages = {},
pmid = {42728335},
issn = {1365-2540},
support = {88887.372011/2019-00 (Fellowhip)//Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (Brazilian Federal Agency for the Support and Evaluation of Graduate Education)/ ; postdoctoral fellowship//Damon Runyon Cancer Research Foundation (Cancer Research Fund of the Damon Runyon-Walter Winchell Foundation)/ ; },
abstract = {Chromosome segregation in eukaryotes requires the orchestrated interaction of chromosomes with microtubules, mediated by the kinetochore multiprotein complex that assembles on chromosomal regions known as centromeres. In most eukaryotes, CenH3 and Cenp-C centromeric proteins are essential for centromere function. In Drosophila, the localization of CenH3 (or Cid in Drosophila) depends on its chaperone CAL1 and Cenp-C. Previous studies have shown that both Cid and Cenp-C underwent a coincident gene duplication and likely functional specialization in the Drosophila subgenus. Independently, Cid duplications led to three paralogs in the montium group (Sophophora subgenus). Here, we investigated whether this group also underwent parallel Cenp-C duplications by analyzing sequenced genomes of 23 montium group species. We identified Cenp-C genes in five distinct syntenic loci. Despite their distinct synteny, all but two montium group species (except D. birchii and D. vulcana) encode a single Cenp-C, whose phylogeny mirrors the species phylogeny, and all encode protein motifs indicative of intact Cenp-C function. These Cenp-C genes resulted from gene translocations or duplication followed by loss of the ancestral copy. Therefore, the co-retention of three Cid paralogs in the montium group did not result in coincident Cenp-C paralog co-retention. Analysis of the selective constraints in Cenp-C reveals more prominent positive selection in the Drosophila subgenus (with two retained Cenp-C paralogs) than in the Sophophora subgenus, including the montium group. Our work highlights differences in functional retention and potential specialization of CenH3 and Cenp-C, two of the most conserved eukaryotic centromeric proteins in Drosophila.},
}

@article {pmid42728894,
year = {2026},
author = {Amberson, T and Shannon Dorcy, K and Sheffield, P and Gallegos, D and Laing, SS},
title = {Utilization of Rapid Qualitative Analysis to Evaluate Intervention Acceptability, Usefulness, and Ease of Implementation in a Community Health Center.},
journal = {Journal of primary care & community health},
volume = {17},
number = {},
pages = {21501319261485527},
pmid = {42728894},
issn = {2150-1327},
support = {T42 OH008433/OH/NIOSH CDC HHS/United States ; },
mesh = {Humans ; Qualitative Research ; Focus Groups ; *Community Health Centers/organization & administration ; Workflow ; *Health Personnel/psychology ; Interviews as Topic ; Leadership ; },
abstract = {ObjectivesTo provide a case example of the use of rapid qualitative analysis (RQA) method to evaluate intervention acceptability, usefulness, and ease of implementation to support healthcare worker well-being in a community health center. We demonstrate steps of the RQA method with data from the workflow redesign evidence-based intervention.MethodsFour semi-structured focus groups were conducted on Zoom with healthcare workers of different occupations (N=22) between March - May 2025. Interviews were recorded and transcribed verbatim. Qualitative data were analyzed using RQA. Trustworthiness of findings was assured with three analysts.ResultsThe RQA methodology facilitated in depth exploration of findings in an expedited time frame, aligning with the immediate goal of identifying supportive measures for healthcare workers. RQA optimized the momentum of change to be collaborative with healthcare workers and leadership. Workflow redesign was consistently identified by participants as an acceptable and useful intervention to improve well-being, with emphasis on the importance of leadership support, resource allocation, and active involvement of frontline healthcare staff in all phases of intervention development and implementation.ConclusionsWe used RQA to analyze qualitative data to provide timely, actionable insights that continue to inform the development, implementation, and tailoring of interventions to support healthcare worker well-being in this community health center. Participants highlighted early staff involvement, clear communication between staff and leadership, and clarity of objectives/purpose to support intervention implementation.},
}

Humans
Qualitative Research
Focus Groups
*Community Health Centers/organization & administration
Workflow
*Health Personnel/psychology
Interviews as Topic
Leadership

@article {pmid42733538,
year = {2026},
author = {Fleury, I and Hill, BT and Eyre, TA and Ujjani, C and Manzoor, BS and Brown, JR and Tuncer, HH and Lamanna, N and Coombs, CC and Ghosh, N and Leslie, LA and Roeker, LE and Martinez-Calle, N and Barr, PM and Davids, MS and Emechebe, N and Rhodes, JM and Skarbnik, AP and Sinai, W and Pearson, L and Lansigan, F and Choi, Y and Jensen, CE and Fakhri, B and Thompson, MC and Stephens, DM and Schuster, SJ and Coyle, M and Chang, A and Kaddis, N and Pivneva, I and Guerin, A and Shadman, M},
title = {Fixed-treatment duration venetoclax following covalent BTKi progression in chronic lymphocytic leukemia.},
journal = {Blood neoplasia},
volume = {3},
number = {4},
pages = {100277},
pmid = {42733538},
issn = {2950-3280},
}

@article {pmid42735368,
year = {2026},
author = {Gajra, A and Zhen, DB and Chiorean, EG},
title = {Bridging the Gap: Precision Oncology for Cancers of Unknown Primary.},
journal = {Journal of clinical oncology : official journal of the American Society of Clinical Oncology},
volume = {},
number = {},
pages = {JCO2601847},
doi = {10.1200/JCO-26-01847},
pmid = {42735368},
issn = {1527-7755},
}

@article {pmid42678905,
year = {2026},
author = {Mowrer, C and Whitsel, EA and Collins, JM and Chen, S and Ekanayaka, A and Manson, JE and Meliker, JR and Reiner, AP and Schwartz, GG and Shadyab, AH and Shi, C and Smith, RL and Stewart, JD and Venkatachalam, HH and Bozigar, M},
title = {Residential Radon Concentration and the Risk of Malignant Brain and Central Nervous System Cancer in US Postmenopausal Women.},
journal = {Neuroepidemiology},
volume = {},
number = {},
pages = {1},
pmid = {42678905},
issn = {1423-0208},
support = {75N92021D00002/HL/NHLBI NIH HHS/United States ; 75N92021D00005/WH/WHI NIH HHS/United States ; T32 ES007018/ES/NIEHS NIH HHS/United States ; R01 ES034050/ES/NIEHS NIH HHS/United States ; 75N92021D00001/HL/NHLBI NIH HHS/United States ; 75N92021D00003/WH/WHI NIH HHS/United States ; 75N92021D00004/WH/WHI NIH HHS/United States ; },
abstract = {BACKGROUND: Central nervous system (CNS) cancers, including brain cancer, are rare but highly lethal, and risk factors remain poorly understood. Radon, a known lung carcinogen, may affect non-pulmonary sites, including the CNS.

METHODS: We estimated the radon-related hazard of incident malignant CNS cancer in a large US cohort of postmenopausal women from the Women's Health Initiative. Incident CNS cancers were identified through physician adjudication or death certificates. Radon concentration estimates at residential addresses included US Geological Survey (USGS) Radon Index and Zones, US Environmental Protection Agency (EPA) Radon Zones, and models from the Lawrence Berkeley National Laboratory (LBL) and Li et al. Cox proportional hazards models were used to estimate hazard ratios, including study design, sociodemographic, behavioral, and environmental covariates. Corresponding population attributable fractions were calculated.

RESULTS: Over follow-up (mean = 17.7 years), 451 incident malignant CNS cancers were identified among 159,391 participants. Absolute risks of malignant CNS cancer increased with increasing radon concentration across all metrics. Nonlinear spline models for USGS Radon Index, LBL estimates, and Li et al. estimates showed increasing CNS hazard even at low radon concentrations (global test of spline terms p = 0.022 for Li et al.). In categorical analyses, the hazard ratio comparing the highest versus lowest Li et al. tertile was 1.49 (95% CI: 1.12-1.99), and the population attributable fraction was 20.1% (4.8%-33.9%).

CONCLUSION: Higher radon concentrations were consistently associated with elevated malignant CNS cancer hazard, with the clearest concentration-response observed in continuous models. Residential radon exposure may contribute meaningfully to the overall burden of CNS cancers in this largest cohort study of the radon-CNS cancer association to date.},
}

@article {pmid42727232,
year = {2026},
author = {Domenjo-Vila, E and Gavin, MA and Prlic, M},
title = {I am me and my circumstance - Context dictates the outcome of IL-1 signaling in and around T cells.},
journal = {Seminars in immunology},
volume = {84},
number = {},
pages = {102065},
doi = {10.1016/j.smim.2026.102065},
pmid = {42727232},
issn = {1096-3618},
support = {R01 AI123323/AI/NIAID NIH HHS/United States ; R01 AI179712/AI/NIAID NIH HHS/United States ; },
}

@article {pmid42726173,
year = {2026},
author = {Lin, T and Guo, B and Bandera, VM and Liesenfeld, DB and Shen, J and Haaland, B and Stewart, PA and Boucher, KM and Erickson, PA and Hardikar, S and Damerell, V and Byrd, DA and Figueiredo, JC and Toriola, AT and Shibata, D and Siegel, EM and Li, CI and Ulrich, AB and Kahlert, C and Scharfstein, DO and Gigic, B and Ulrich, CM and Ose, J},
title = {Urinary metabolomics may improve prediction of overall survival beyond tumor stage in colorectal cancer: results from the ColoCare study.},
journal = {Metabolomics : Official journal of the Metabolomic Society},
volume = {22},
number = {5},
pages = {},
pmid = {42726173},
issn = {1573-3890},
mesh = {Humans ; *Colorectal Neoplasms/urine/pathology/metabolism/mortality/diagnosis ; *Metabolomics/methods ; Prognosis ; Female ; Neoplasm Staging ; Male ; *Biomarkers, Tumor/urine ; Aged ; Middle Aged ; },
abstract = {BACKGROUND: Colorectal cancer (CRC) is a leading cause of cancer-related mortality. Prognosis is primarily guided by tumor stage despite substantial molecular heterogeneity. Urinary metabolomics may capture systemic and tumor-related biology beyond staging and could improve prognostic assessment. We hypothesized that incorporating urinary metabolomic profiles would improve overall survival (OS) prediction performance compared with a stage- and age-based reference model.

METHOD: A total of n = 76 stage I-IV CRC patients recruited as part of the ColoCare Study in Heidelberg Germany with pre-surgery urinary metabolomics were included (23 deaths; median follow-up 3.03 years). Four metabolomics-based penalized Cox models adjusted for tumor stage and age at diagnosis were developed using LASSO, adaptive LASSO, spike-and-slab LASSO, and iterative sure independence screening (iSIS)-LASSO. Model discrimination was assessed using Harrell's C-index and time-dependent AUC based on the nested cross-validation.

RESULTS: Compared with the reference model (Cox model including only tumor stage and age at diagnosis), all metabolomics-based models provided better discrimination. The spike-and-slab LASSO Cox model demonstrated the best performance, achieving a C-index of 0.75 (vs. 0.68) and consistently higher time-dependent AUCs at 1-5 years of follow-up, with a peak AUC of 0.76 at year 3 (vs. 0.68). Three urinary metabolites were consistently selected across all metabolomics-based models: indolelactate, 2-hydroxyisobutyrate and a uridine-like metabolite.

CONCLUSIONS: Urinary metabolomics may improve CRC OS prediction beyond tumor stage and age at diagnosis, especially with the spike-and-slab LASSO Cox model. These results support urinary metabolomics as a promising noninvasive prognostic tool that merits external validation.},
}

Humans
*Colorectal Neoplasms/urine/pathology/metabolism/mortality/diagnosis
*Metabolomics/methods
Prognosis
Female
Neoplasm Staging
Male
*Biomarkers, Tumor/urine
Aged
Middle Aged

@article {pmid42726603,
year = {2026},
author = {Victor, T and Barnes, G and Shadman, M and Lamanna, N and Tam, CS and Qiu, L and Salmi, T and Barnes, FB and Korde, R and Brown, JR},
title = {Association between patient-reported symptoms and clinical outcomes in R/R CLL.},
journal = {Blood advances},
volume = {},
number = {},
pages = {},
doi = {10.1182/bloodadvances.2026020405},
pmid = {42726603},
issn = {2473-9537},
abstract = {The ALPINE trial was a randomized, open-label study comparing the efficacy and safety of zanubrutinib versus ibrutinib monotherapy in patients with relapsed/refractory chronic lymphocytic leukemia/small lymphocytic lymphoma (R/R CLL/SLL). Using patient-reported outcome (PRO) data from the ALPINE trial, the current study aimed to investigate the association between disease-specific patient-reported symptoms and the clinical outcomes of progression-free survival (PFS) and duration of response (DoR). After adjusting for baseline stratification factors, zanubrutinib was associated with lower PRO-based recurrent symptomatic deterioration compared to ibrutinib. Zanubrutinib also demonstrated significantly lower risk of disease progression and better DoR across all disease-specific patient-reported symptoms. Compared to ibrutinib, zanubrutinib demonstrated a 28%-33% reduction in the risk of a PFS event after adjusting for global health status, physical functioning, role functioning, fatigue, pain, nausea and vomiting, diarrhea, and constipation (all P < .02). Similarly, zanubrutinib demonstrated a 31%-51% reduced risk of shortened DoR after adjusting for the patient-reported scores (all P < .02). These are crucial aspects in clinical decision-making, as they highlight zanubrutinib's association with improved clinical outcomes and patient-reported symptomatology. These findings reinforce the enhanced efficacy profile of zanubrutinib in patients with R/R CLL/SLL by demonstrating its lower patient-reported symptom deterioration in addition to increased PFS and better DoR.},
}

@article {pmid42727064,
year = {2026},
author = {Swanepoel, C and Fourment, M and Ji, X and Nasif, H and Suchard, MA and Iv, FAM and Drummond, AJ},
title = {TreeFlow: Probabilistic Modelling and Automatic Differentiation for Phylogenetics.},
journal = {Systematic biology},
volume = {},
number = {},
pages = {},
doi = {10.1093/sysbio/syag072},
pmid = {42727064},
issn = {1076-836X},
abstract = {Probabilistic modelling frameworks are powerful tools for statistical modelling and inference. They are not immediately generalizable to phylogenetic problems due to the particular computational properties of the phylogenetic tree object. TreeFlow is a software library for probabilistic modelling and automatic differentiation with phylogenetic trees. It embeds phylogenetic trees in the TensorFlow Probability framework, and implements inference algorithms for phylogenetic models given a fixed tree topology. We demonstrate how TreeFlow can be used to quickly implement and assess new models. We also show that it provides reasonable performance for gradient-based inference algorithms compared to specialized computational libraries for phylogenetics.},
}

@article {pmid42725863,
year = {2026},
author = {Wu, L and Anderson, PL and MaWhinney, S and Saina, M and Mugo, NR and Brown, CE and Akelo, N and Thomas, K and Morton, JF and Hill, E and Ngure, K and Rechkina, EA and Bushman, L and Donnell, D and Mugwanya, KK and , },
title = {Effect of Pregnancy on Intracellular Tenofovir Diphosphate Exposure and Thresholds following Oral Emtricitabine-Tenofovir Disoproxil fumarate Pre-Exposure Prophylaxis: A Directly Observed Dosing Study.},
journal = {The Journal of infectious diseases},
volume = {},
number = {},
pages = {},
doi = {10.1093/infdis/jiag460},
pmid = {42725863},
issn = {1537-6613},
abstract = {INTRODUCTION: Intraerythrocytic tenofovir diphosphate (TFV-DP) concentrations from emtricitabine/tenofovir disoproxil fumarate (F/TDF) pre-exposure prophylaxis (PrEP) measured in dried blood spots (DBS) are ∼30-40% lower during pregnancy, but data on TFV-DP concentrations in peripheral blood mononuclear cells (PBMCs) are limited. We evaluated the effect of pregnancy on intracellular TFV-DP concentrations in PBMCs.

METHODS: Directly observed dosing (DOD) of daily oral F/TDF was administered to 18 healthy non-pregnant and 18 pregnant Kenyan women without HIV for eight weeks. Blood for DBS and PBMC was collected weekly for non-pregnant and bi-weekly for pregnant women. TFV-DP concentrations in DBS and PBMCs were quantified using validated liquid chromatography-tandem mass spectrometry. Steady-state fitted TFV-DP concentrations in PBMC and DBS were compared between pregnant and non-pregnant women.

RESULTS: Median (IQR) age was 23 (20-27) years and gestational age was 16 (14-20) weeks for pregnant women at enrollment. Median (IQR) Cockroft Gault-estimated creatinine clearance was 131 (113-146) mL/Min for non-pregnant versus 176 (154-196) mL/Min for pregnant women. 1922 of 1925 (99.8%) expected doses were directly observed. Fitted steady-state median (IQR) TFV-DP concentrations in DBS were 1545 (1203, 1887) fmol/punch in non-pregnant versus 919 (835, 1003) fmol/punch in pregnant women [percent change: 40.5%, 95%CI (29.5%, 51.5%); p<0.001]. Modeled steady-state geometric mean (95%CI) PBMC TFV-DP concentrations were 56.2 (48.0, 65.8) fmol/106 cells in non-pregnant versus 47.8 (40.4, 56.5) fmol/106 cells in pregnant women [geometric mean ratio (GMR, 95%CI): 0.85 (0.68, 1.06); p=0.15].

CONCLUSION: Steady-state TFV-DP concentrations in PBMCs were reassuringly not meaningfully different between pregnant and non-pregnant women.},
}

@article {pmid42725700,
year = {2026},
author = {Oeschger, TM and Varco-Merth, B and Starke, CE and Poole, NH and Reddy, SS and Cruz, A and Medina, M and Dannay, R and Singh, SP and Nekorchuk, M and Swanson, T and McAllister, R and Bochart, R and Labriola, C and Magnani, DM and Olson, JM and Price, JP and Estes, JD and Peterson, CW and Okoye, AA},
title = {Chimeric Antigen Receptor T Cell Targeting of Natural Killer Cells in Peripheral Blood and Tissues of Rhesus Macaques.},
journal = {Human gene therapy},
volume = {},
number = {},
pages = {10430342261486115},
doi = {10.1177/10430342261486115},
pmid = {42725700},
issn = {1557-7422},
abstract = {Natural killer (NK) cells lead a rapid and potent innate immune response following exposure to infectious agents, but their activity may also contribute to chronic inflammation and augmented disease pathogenesis. Previous reports have shown that Janus kinase 3 inhibitors or anti-IL-15 monoclonal antibodies potently deplete NK cells in nonhuman primates (NHPs). However, they also disrupt T cell homeostasis, making it difficult to use these reagents to delineate the nonredundant role of NK cells in NHPs. To induce the specific depletion of NK cells in vivo, we designed chimeric antigen receptor (CAR) T cells targeting either a broad (CD16[+]) or narrow (NKG2A/C[+]) proportion of NK-inclusive innate immune subsets in rhesus macaques (RM). Ex vivo screening assays identified anti-CD16 and anti-NKG2A/C CAR constructs that potently and specifically depleted CD16[+] and NKG2A/C[+] cells, respectively, in the presence of autologous peripheral blood mononuclear cells (PBMCs). Adoptive transfer of autologous anti-NKG2A/C CARs was associated with a profound depletion of NK cells in blood and tissues of RM. NK cell depletion occurred despite modest anti-NKG2A/C CAR T cell expansion and persistence. No target cell depletion was observed following anti-CD16 CAR T-cell infusion, potentially due to the CAR T-cell dose and/or infusion frequency, animal-specific factors, or limitations of the CAR construct. Collectively, our pioneering study expands the application of CAR T cells as a basic science tool and further advances the NHP model for studying NK cell activity in disease contexts, such as infectious diseases and allotransplantation.},
}

@article {pmid42722204,
year = {2026},
author = {Guan, F and Stewart, RD and Carlson, DJ},
title = {A mechanism-guided approach for quantifying the biological effects of tumor hypoxia in particle therapy.},
journal = {International journal of radiation oncology, biology, physics},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.ijrobp.2026.09.004},
pmid = {42722204},
issn = {1879-355X},
abstract = {PURPOSE: To quantify how acute tumor hypoxia modifies the biological effectiveness of proton, helium, and carbon ions and to derive mechanistic hypoxia-compensation factors for representative spread-out Bragg peaks (SOBPs).

METHODS: The Monte Carlo Damage Simulation (MCDS) was used to generate DNA double-strand break (DSB) yields as functions of radiation quality q = (Zeff/β)[2] and oxygen level pO2 (0.0001-100%). MCDS-derived DSB yields were integrated into Geant4 Monte Carlo simulations, and Repair-Misrepair-Fixation (RMF) model calculations were used to derive linear-quadratic radiosensitivity parameters. We distinguish hypoxic RBE (RBEH), which compares the biological effects of particles at reduced pO2 with photons under normoxic conditions ([137]Cs γ-rays at pO2 = 100%), from isoeffective RBE (RBEiso), which compares particles and photons at the same pO2. SOBP (10-15 cm depth) optimizations used either a uniform 2 Gy absorbed dose or a uniform RBEH-weighted dose (DRBE = 3.8 Gy) corresponding to 10% clonogenic survival in H460 cells; hypoxia reduction factors (HRFs) quantified the absorbed-dose compensation required to preserve this modeled endpoint.

RESULTS: At pO2 = 21%, at DRBE = 3.8 Gy, RBEH was 1.04-1.16 for protons, 1.23-1.67 for helium ions, and 1.84-3.55 for carbon ions. At pO2 = 0.001%, RBEH decreased to 0.39-0.41, 0.50-0.70, and 0.87-2.28, respectively. Because RBEH uses the fixed photon reference at pO2 = 100%, values below unity quantify the combined oxygen and radiation-quality penalty and do not indicate that particles are less effective than photons irradiating the same hypoxic tissue. At pO2 = 0.001%, RBEiso remained >1 (protons 1.13-1.19; helium 1.46-2.03; carbon 2.54-6.63). The corresponding HRFs were 2.73-2.89, 2.42-2.53, and 1.57-2.07.

CONCLUSION: Within the H460 single-fraction clonogenic-survival framework examined here, high-LET carbon ions are less sensitive to severe hypoxia than helium ions or protons and require smaller model-derived hypoxia-compensation factors.},
}

@article {pmid42722536,
year = {2026},
author = {Elitzur, S and Cai, J and Heyman, MM and Hunger, SP and Inaba, H and Karol, SE and Loh, ML and Manabe, A and Pieters, R and Pui, CH and Rizzari, C and Silverman, LB and Teachey, DT and Schrappe, M},
title = {The 21st International ``Ponte di Legno'' Childhood Acute Lymphoblastic Leukemia Workshop Report: Progress and Emerging Opportunities.},
journal = {Clinical lymphoma, myeloma & leukemia},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.clml.2026.08.009},
pmid = {42722536},
issn = {2152-2669},
abstract = {The 21st Ponte di Legno Working Group meeting convened in Orlando, USA, on December 4-5, 2025, bringing together leading childhood acute lymphoblastic leukemia (ALL) investigators from major global consortia. In response to the transformative advances in childhood ALL treatment, particularly the integration of immunotherapy into frontline therapy, the group revisited and updated its mission statement. The revised mission emphasizes collaborative studies on rare leukemia subsets, harmonized toxicity reporting, particularly for immunotherapy-related toxicities, and unrestricted worldwide collaboration. In addition, sharing data and strategies for integrating novel agents will be integral to optimizing future trial design. Key scientific topics included rare genetic subgroups, T-cell ALL genomics, treatment-related toxicity benchmarking, and central nervous system (CNS) disease management challenges. A major focus was immunotherapy integration into frontline therapy, particularly blinatumomab as an emerging standard of care and inotuzumab ozogamicin as an investigational agent, and their potential to enable chemotherapy de-escalation. Additional discussions addressed immunotherapy-specific toxicities. The integration of immunotherapy into frontline ALL therapy represents a paradigm shift with potential to improve outcomes while reducing treatment burden. However, careful attention to CNS disease control, emerging toxicities, and preservation of the remarkable achievements in childhood ALL therapy remains essential as the field advances.},
}

@article {pmid42723524,
year = {2026},
author = {Demedis, J and Stratton, KL and Leisenring, WM and Brinkman, TM and Howell, RM and Armstrong, GT and Meacham, LR and Chow, EJ and Marchak, JG},
title = {Male survivors of childhood cancer and perceptions of sexual dysfunction risk: A report from the Childhood Cancer Survivor Study.},
journal = {Cancer},
volume = {132},
number = {18},
pages = {e70599},
pmid = {42723524},
issn = {1097-0142},
support = {U24 CA055727/CA/NCI NIH HHS/United States ; CA21765/CA/NCI NIH HHS/United States ; //American Lebanese Syrian Associated Charities/ ; P30 CA021765/CA/NCI NIH HHS/United States ; //Lance Armstrong Foundation/ ; CA55727/CA/NCI NIH HHS/United States ; },
mesh = {Humans ; Male ; Adult ; *Cancer Survivors/psychology/statistics & numerical data ; Child ; Young Adult ; *Neoplasms/therapy/complications/psychology ; *Sexual Dysfunction, Physiological/etiology/epidemiology/psychology ; Adolescent ; Risk Factors ; Middle Aged ; Infant ; Child, Preschool ; Perception ; Infant, Newborn ; },
abstract = {BACKGROUND: Sexual dysfunction (SD) is an underrecognized late effect of childhood cancer. This study sought to comprehensively examine factors influencing the perceived risk of SD among male survivors of childhood cancer.

METHODS: Adult male survivors (N = 1581) from the Childhood Cancer Survivor Study who were aged a median of 8 years (range, 0-20 years) at cancer diagnosis and 38 years (range, 22-60 years) at survey reported their perceptions of relative risk for SD compared to peers. Multivariable logistic regression evaluated sociodemographic, treatment, and health factors associated with perceptions of risk.

RESULTS: Overall, 29% of survivors (450 of 1581) perceived themselves at increased risk for SD. Among survivors exposed to treatments known to be associated with SD risk, increased risk was perceived by only 33%-42% of males, which varied by the specific exposure. Treatment-related risk factors (vs. no exposure) associated with increased perception included gonadotoxic chemotherapy (odds ratio [OR], 1.6; 95% CI, 1.2-2.1), genitourinary/pelvic/spinal surgery (OR, 2.6; 95% CI, 1.4-4.7), and pelvic/testicular radiation (OR, 1.9; 95% CI, 1.4-2.5). Poor mental health-related quality of life (OR, 2.0; 95% CI, 1.4-2.7) and less-than-excellent general health were associated with increased perception of SD risk. Men who perceived heightened SD risk reported oncologists (26.4%) and primary care providers (25.3%) as top sources of information about risk.

CONCLUSIONS: Many male survivors do not perceive heightened risks for SD, despite a history of treatment-related risk factors. Because SD risk is multifactorial, oncology and survivorship providers should prioritize individualized education and counseling to improve survivors' understanding of their risk on the basis of their treatment history and current health.},
}

Humans
Male
Adult
*Cancer Survivors/psychology/statistics & numerical data
Child
Young Adult
*Neoplasms/therapy/complications/psychology
*Sexual Dysfunction, Physiological/etiology/epidemiology/psychology
Adolescent
Risk Factors
Middle Aged
Infant
Child, Preschool
Perception
Infant, Newborn

@article {pmid42723608,
year = {2026},
author = {Murphy, NR and Triplette, M and Adams, SV and Rustagi, AS and Sigel, K and Butt, AA and Soo Hoo, GW and Kim, JW and Akgün, KM and Crothers, K},
title = {Outcomes of lung cancer screening in a nation-wide cohort of people with HIV compared to without HIV.},
journal = {American journal of respiratory and critical care medicine},
volume = {},
number = {},
pages = {},
doi = {10.1093/ajrccm/aamag448},
pmid = {42723608},
issn = {1535-4970},
}

@article {pmid42715345,
year = {2026},
author = {Asano, Y and Veatch, JR and Sung, CJ and Tang, TH and Mazziotta, F and Natsuki, S and McAfee, M and Bakhtiari, J and Lee, B and Martin, L and Rizzi, A and Zhang, T and Smith, CW and Paulson, KG and Schmitt, TM and Newell, EW and Elz, AE and Chen, DG and Su, Y and Gustafson, HH and Yeung, CCS and Seaton, B and Hunter, D and Koelle, DM and Bhatia, S and Hall, ET and Voillet, V and Cao, J and Gooley, T and Greenberg, PD and Gottardo, R and Oda, SK and Nghiem, P and Chapuis, AG},
title = {Reprogramming engineered autologous T cells to overcome resistance in patients with Merkel cell carcinoma.},
journal = {Science translational medicine},
volume = {18},
number = {866},
pages = {eaea8773},
doi = {10.1126/scitranslmed.aea8773},
pmid = {42715345},
issn = {1946-6242},
support = {P01 CA225517/CA/NCI NIH HHS/United States ; },
mesh = {Animals ; Female ; Humans ; Male ; Mice ; *Carcinoma, Merkel Cell/immunology/therapy/pathology ; Cell Line, Tumor ; *Drug Resistance, Neoplasm ; Merkel cell polyomavirus ; Receptors, Antigen, T-Cell/metabolism ; *T-Lymphocytes/immunology ; },
abstract = {Immune checkpoint inhibitors (ICIs) have transformed Merkel cell carcinoma (MCC) outcomes, but most patients with MCC develop resistance. We identified T cell receptor (TCR)MCC1, a highly avid, HLA-A*02:01-restricted TCR targeting the Merkel cell polyomavirus (MCPyV) oncoprotein large-T antigen15-23. Seven patients with ICI-refractory metastatic MCPyV[+] MCC received TCRMCC1-transduced cells (TTCR-MCC1 cells) after lymphodepleting chemotherapy or HLA-enhancing interventions [radiation or interferon gamma-1b (Actimmune)], with concurrent ICIs (NCT03747484). TTCR-MCC1 cells trafficked to tumor sites and expressed a gene expression profile compatible with T cell activation, with tumor regression observed in two patients. However, therapeutic activity was limited by HLA class I silencing, a common mechanism of immune escape in MCC. In one patient, delayed tumor regression coincided with endogenous effector immune activation and restoration of MCC HLA expression, implying that robust local responses could reverse HLA silencing. To overcome this barrier, we engineered CD4 and CD8 TTCR-MCC1 cells to coexpress CD8αβ and a CD200R-CD28 switch receptor, enabling CD4 T cell engagement and T cell costimulation. These modifications enhanced tumor infiltration, increased HLA expression, and improved control of HLA[low] MCC in vivo in mice. These findings support the feasibility of TCR-engineered cell therapy for MCPyV[+] MCC and provide a blueprint for overcoming immune evasion via targeted localized enhancement of antigen presentation.},
}

Animals
Female
Humans
Male
Mice
*Carcinoma, Merkel Cell/immunology/therapy/pathology
Cell Line, Tumor
*Drug Resistance, Neoplasm
Merkel cell polyomavirus
Receptors, Antigen, T-Cell/metabolism
*T-Lymphocytes/immunology

@article {pmid42715569,
year = {2026},
author = {Steffin, D and Courtney, AN and Choe, M and Ghatwai, N and Esparza Cerda, MA and Sweidan, R and Dhanashree, R and Zhang, H and Lapteva, N and Mei, Z and Grilley, BJ and Metelitsa, LS and Heslop, HE and Brenner, MK and Heczey, A},
title = {Complete Regression of Hepatoblastoma after Interleukin-15- and Interleukin-21-Coexpressing CAR T-Cell Therapy.},
journal = {The New England journal of medicine},
volume = {395},
number = {10},
pages = {1029-1032},
doi = {10.1056/NEJMc2605958},
pmid = {42715569},
issn = {1533-4406},
support = {RP240545//Cancer Prevention and Research Institute of Texas/ ; HSN261201500003I, 75N92019D00018 and HSN2612015000/NH/NIH HHS/United States ; P50CA126752/NH/NIH HHS/United States ; R01CA258866/NH/NIH HHS/United States ; },
}

@article {pmid42716341,
year = {2026},
author = {Shadman, M and Ahlstrom, J and Gutierrez, M and Nastoupil, L and Porter, D and Schmitt, A and Zitella, L and Graff, T},
title = {Barriers to Patient Referral and Completion of CAR T-Cell Therapy for Relapsed/Refractory Large B-Cell Lymphoma.},
journal = {Transplantation and cellular therapy},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.jtct.2026.09.010},
pmid = {42716341},
issn = {2666-6367},
abstract = {Chimeric antigen receptor (CAR) T-cell therapy has improved outcomes for patients with hematologic malignancies such as relapsed or refractory large B-cell lymphoma. However, research indicates that a substantial proportion of medically eligible patients with relapsed or refractory large B-cell lymphoma in the United States do not receive CAR T-cell therapy. Multiple barriers across the treatment pathway contribute to the significant gap between patient eligibility and receiving treatment. To further examine these barriers, a multistakeholder panel was convened on October 8, 2025. Key barriers identified included limited patient awareness of CAR T-cell therapy, inadequate knowledge and application of eligibility criteria, logistical and financial burdens, and delays resulting from health system processes. The panel members identified potential ways to improve treatment access and completion, including expanding treatment sites capable of delivering CAR T-cell therapy in community settings and shifting supportive resources (financial counselors, social workers, patient navigators) from treatment centers to community oncology practices.},
}

@article {pmid42718812,
year = {2026},
author = {Kuo, SH and Sharma, J and Wu, C and Vieson, MD and Kosmider, B and Randell, SH and Nanjappa, SG and Lau, GW},
title = {Pseudomonas aeruginosa-derived volatile organic compounds modulate host immunity to disrupt airway mucus homeostasis.},
journal = {Frontiers in immunology},
volume = {17},
number = {},
pages = {1823251},
pmid = {42718812},
issn = {1664-3224},
support = {P30 DK065988/DK/NIDDK NIH HHS/United States ; R01 HL142626/HL/NHLBI NIH HHS/United States ; R21 AI171524/AI/NIAID NIH HHS/United States ; },
mesh = {Animals ; *Pseudomonas aeruginosa/immunology/metabolism ; Humans ; *Volatile Organic Compounds/metabolism/immunology ; *Mucus/metabolism/immunology ; *Pseudomonas Infections/immunology/metabolism/microbiology ; Mice ; Homeostasis ; *Respiratory Mucosa/immunology/metabolism ; Interleukin-17/metabolism ; Host-Pathogen Interactions/immunology ; Macrophages/immunology/metabolism ; Epithelial Cells/immunology/metabolism ; },
abstract = {Chronic pulmonary diseases, including cystic fibrosis, chronic obstructive pulmonary disease, and chronic bronchitis, as well as ventilator-associated pneumonia, are characterized by persistent infection of mucus-laden airways. Pseudomonas aeruginosa (PA) is a dominant pathogen in these conditions and produces volatile organic compounds (VOCs) that have been proposed as biomarkers of disease exacerbation; however, their immunopathogenic roles remain unclear. We investigated PA-derived VOCs using human bronchial epithelial air-liquid interface cultures and murine models. VOCs exposure significantly increased airway mucin expression and induced a proinflammatory response characterized by M1 macrophage polarization (iNOS[+]), neutrophil recruitment, and expansion of IL-17A-producing Thy1.2[+] lymphocytes. Functional depletion of macrophages, neutrophils, or IL-17A in vivo each attenuated mucin production and goblet cell metaplasia, indicating non-redundant contributions to mucus pathology. In vitro, IL-17A neutralization partially restored FOXA2 expression and reduced mucin production, supporting a role in mucus regulation. On the mechanistic level, we discovered an IL-17A-dependent dual-axis pathway involving both epithelial cell-mediated autocrine and lymphocyte-mediated paracrine signaling that contributes to the feed-forward loop of inflammation and enhances the signaling pathways regulating mucus hypersecretion in airways. We conclude that PA VOCs activate multiple proinflammatory responses to convergently drive mucus pathogenesis in the diseased lung.},
}

Animals
*Pseudomonas aeruginosa/immunology/metabolism
Humans
*Volatile Organic Compounds/metabolism/immunology
*Mucus/metabolism/immunology
*Pseudomonas Infections/immunology/metabolism/microbiology
Mice
Homeostasis
*Respiratory Mucosa/immunology/metabolism
Interleukin-17/metabolism
Host-Pathogen Interactions/immunology
Macrophages/immunology/metabolism
Epithelial Cells/immunology/metabolism

@article {pmid42718825,
year = {2026},
author = {Novin, S and Holt, SK and Swaminathan, M and Wright, J and Gore, J and Hyrich, K and Zhao, SS and Sparks, J and Makris, U and Suarez-Almazor, M and Grivas, P and Psutka, S and Singh, N},
title = {Association between rheumatoid arthritis, frailty status, mortality and anti-cancer therapy: a retrospective SEER-Medicare analysis in patients with non-metastatic renal cell carcinoma.},
journal = {Annals of translational medicine},
volume = {14},
number = {4},
pages = {47},
pmid = {42718825},
issn = {2305-5839},
support = {HHSN261201800032C/CA/NCI NIH HHS/United States ; R03 AG082857/AG/NIA NIH HHS/United States ; HHSN261201800015I/CA/NCI NIH HHS/United States ; R01 AR078484/AR/NIAMS NIH HHS/United States ; HHSN261201800032I/CA/NCI NIH HHS/United States ; HHSN261201800015C/CA/NCI NIH HHS/United States ; HHSN261201800009I/CA/NCI NIH HHS/United States ; K23 AR079588/AR/NIAMS NIH HHS/United States ; HHSN261201800009C/CA/NCI NIH HHS/United States ; },
abstract = {BACKGROUND: Renal cell carcinoma (RCC) patients with rheumatoid arthritis (RA) represent a niche but understudied population that often suffers from comorbid frailty. Frailty and RA may adversely affect treatment and mortality outcomes in patients with cancer. We aim to evaluate the association between RA and mortality/treatment outcomes in patients with RCC, with attention to the impact of frailty on these associations.

METHODS: Retrospective cohort study examining patients aged 65 and older, with Medicare part A and B coverage and non-metastatic clear cell renal cell carcinoma (ccRCC) diagnosed between 2004-2017 via the Surveillance Epidemiology and End Results (SEER)-Medicare database. Patients stratified by RA, defined by having 2 or more ICD-9 and ICD-10 codes 30 to 365 days apart, and frailty status with a score of ≥0.25 using a validated claims-based frailty index (Kim et al. 2018). Receipt of immunotherapy and cancer-related surgery were assessed and compared. Cox proportional hazards regression models evaluated the association between RA, frailty and mortality (all-cause and cancer-specific). Competing risk analysis using fine-gray model used to assess interaction between RA and frailty with mortality.

RESULTS: The population included 31,989 patients, of which 802 patients had RA and 3,918 were frail. Approximately 60% of the population was male. Rates of cancer-related surgery were not significantly changed by RA status. No significant difference in immunotherapy administration based on RA status was observed [odds ratio (OR) 0.81, 95% confidence interval (CI): 0.59-1.12]. Frailty modified the relationship between RA and all-cause mortality (P=0.01). RA was associated with higher all-cause mortality risk in non-frail patients [hazard ratio (HR) 1.15, 95% CI: 1.03-1.29], but no difference in risk in frail patients (HR 0.94, 95% CI: 0.79-1.14). Frailty was associated with a higher risk of cancer-specific mortality (HR 1.37, 95% CI: 1.26-1.50), while RA was not (HR 1.08, 95% CI: 0.91-1.29).

CONCLUSIONS: RA was an independent risk factor for all-cause mortality in non-frail patients with non-metastatic ccRCC, but not in frail patients. Frailty interacts with RA on the risk of all-cause mortality in this population. The presence of frailty, but not RA, was an independent risk factor for cancer-specific mortality. RA did not appear to significantly impact the receipt of immunotherapy and cancer-related surgery. The complex contributions of frailty and RA to mortality underscore the need for interdisciplinary collaboration between rheumatologists and oncologists in order to maximize treatment and mortality outcomes.},
}

@article {pmid42719791,
year = {2026},
author = {Narasimhan, RM and Levy, MS and Blanco, M and Dreyfuss, IB and Krc, RF and Corriher, TJ and Mashayekhi, M and Ponce, SB and Lichter, K and Caldwell, AI and Jagsi, R and Kahn, JM and Wong, W and Masters, A and Yorke, AA and Taswell, CS},
title = {The Society for Women in Radiation Oncology Medical Physicists: Where Are We Five Years Later?.},
journal = {Cureus},
volume = {18},
number = {8},
pages = {e114277},
pmid = {42719791},
issn = {2168-8184},
abstract = {Background A better understanding of the personal experiences of women and gender minorities in medical physics is needed to ensure the vitality of the radiation oncology (RO) workforce. Founded in 2017, the Society for Women in Radiation Oncology (SWRO) sought to promote gender equity in RO and includes both physician and medical physicist members. Methods From January to February 2023, an anonymous 82-question survey was conducted among all current SWRO members, including both physicians and medical physicists, via the SWRO email listserv. Survey questions covered demographics, family planning, mentorship, well-being, perceptions of SWRO membership, and perceptions of the RO field. A sub-analysis was performed on the survey responses from medical physicists. Descriptive statistics were utilized to summarize the findings. Results In this sub-analysis of physicists, 20 of 26 physicist members (77% participation rate), including 15 medical physicists and five resident physicists, completed the survey. The majority of survey respondents were in the 31-35 year old age group (35%) and female (95%). The top three limitations of academic productivity reported included clinical responsibilities (34%), insufficient mentorship (26%), and insufficient funding (16%). Twenty-eight percent of respondents reported feeling somewhat or extremely satisfied with the mentorship available at their institution, while 60% reported being somewhat or extremely satisfied with female mentorship in the field. Thirty-nine percent of respondents perceived gender-specific biases or obstacles within their program. Among respondents, 44% reported unwanted sexual comments, attention, or advances by colleagues or superiors. Suggested areas for improvement included increasing education on career development, promoting greater physics representation within SWRO, enhancing integration of physics and RO events, and increasing opportunities for in-person interaction. Conclusion This sub-analysis of a broader SWRO survey presents the perspectives of women and gender minority physicists within RO, highlighting shared opportunities for improvement between RO physicians and physicists regarding female mentorship and gender-based challenges. This supports the importance of organizations such as SWRO in promoting representation and gender equity in RO.},
}

@article {pmid42720616,
year = {2026},
author = {Yadav, H and Cheng, GS and Bergeron, A and Williams, KM and Sheshadri, A},
title = {The Lung Function Score Retains Prognostic Value Under Z-Score-Based Interpretation.},
journal = {Annals of the American Thoracic Society},
volume = {},
number = {},
pages = {},
doi = {10.1093/annalsats/aaoag290},
pmid = {42720616},
issn = {2325-6621},
}

@article {pmid42721221,
year = {2026},
author = {Bansi-Matharu, L and Citron, DT and Martin-Hughes, R and Moolla, H and Stover, J and Pickles, M and Mangal, T and Smith, J and Mugurungi, O and Kubyana, MS and Taramusi, I and Cambiano, V and Mpofu, A and Ten Brink, D and Mudimu, E and Apollo, T and Bershteyn, A and Chewere, L and Dimitrov, D and Macheso, S and Johnson, LF and Phillips, A},
title = {HIV diagnosis and treatment status in individuals dying from HIV in Zimbabwe, Malawi, and South Africa: A model comparison analysis.},
journal = {PLoS medicine},
volume = {23},
number = {9},
pages = {e1004864},
pmid = {42721221},
issn = {1549-1676},
support = {INV-007145//Bill & Melinda Gates Foundation/United States ; UM1 AI068617/AI/NIAID NIH HHS/United States ; },
mesh = {Humans ; Malawi/epidemiology ; Zimbabwe/epidemiology ; *HIV Infections/mortality/drug therapy/diagnosis/epidemiology ; South Africa/epidemiology ; Prevalence ; *Anti-HIV Agents/therapeutic use ; Male ; Female ; Adult ; Young Adult ; },
abstract = {BACKGROUND: Antiretroviral therapy (ART) has greatly reduced HIV-related mortality and improved life expectancy in sub-Saharan Africa since the early 2000s. However, HIV-related mortality remains high. To guide intervention priorities, we used seven established HIV simulation models to identify where in the HIV care cascade deaths occur in Zimbabwe, Malawi, and South Africa. This multi-model approach provided a more comprehensive and robust assessment than could be achieved using any single modelling approach.

METHODS AND FINDINGS: To assess alignment, each model generated key HIV metrics from 2000 to 2045, including total population, HIV prevalence, annual new infections, and proportions of people with HIV (PWH) who were diagnosed, on ART, and virally suppressed. HIV-related deaths were estimated annually and categorised by whether they occurred in individuals who were (1) undiagnosed, (2) diagnosed but had not yet started ART, (3) on ART, or (4) had interrupted ART. The models showed strong consistency with population estimates and HIV prevalence across the different settings. There was, however, variation in the absolute number of HIV-related deaths between models; in Zimbabwe in 2025, this ranged from 3,666 to 17,475; in Malawi from 4,580 to 17,835; and in South Africa from 39,470 to 114,968. In Zimbabwe, all models consistently indicated that PWH receiving ART made up the largest proportion of HIV-related deaths, though this proportion differed across models, ranging from 35% to 64%. This was followed by HIV-related deaths amongst those who had interrupted ART, ranging from 17% to 29%. Similar trends were seen in Malawi. In South Africa, a high proportion of HIV-related deaths occurred amongst people who had interrupted ART (23% to 74% in 2025) as well as those who were currently receiving ART (23% to 56%). Models are reliant on empirical data and limited data availability-in this instance, lack of national death registries-is a key constraint on modelling studies.

CONCLUSION: Absolute numbers of HIV-related deaths vary substantially between models, highlighting wider issues around ascertainment of death in the region. However, our results do consistently show that most deaths are occurring amongst PWH on ART in Zimbabwe and Malawi, and amongst those who have interrupted treatment in South Africa, suggesting interventions around adherence counselling and retention in care need to be prioritised.},
}

Humans
Malawi/epidemiology
Zimbabwe/epidemiology
*HIV Infections/mortality/drug therapy/diagnosis/epidemiology
South Africa/epidemiology
Prevalence
*Anti-HIV Agents/therapeutic use
Male
Female
Adult
Young Adult

@article {pmid42721579,
year = {2026},
author = {Xu, H and Yu, G and Lu, Y and Fuller, H and Song, S and Shen, Y and Chiang, CWK and Darst, BF and Ye, K},
title = {Polygenic predisposition modifies the associations of fish oil supplementation with circulating omega-3 fatty acids: A cross-sectional gene-diet interaction study.},
journal = {Clinical nutrition (Edinburgh, Scotland)},
volume = {65},
number = {},
pages = {106774},
doi = {10.1016/j.clnu.2026.106774},
pmid = {42721579},
issn = {1532-1983},
abstract = {BACKGROUND AND AIMS: Several genetic variants have been identified to modify the effects of fish oil supplementation (FOS) on increasing circulating omega-3 fatty acids, but it remains unexplored whether polygenic predisposition to low circulating omega-3 fatty acids modifies these effects. This study aims to test if polygenic scores (PGS) for circulating omega-3 fatty acids modify the associations of FOS with corresponding circulating concentrations.

METHODS: We developed PGS models for absolute circulating concentrations of total omega-3 fatty acids (Omega-3), docosahexaenoic acid (DHA), and their relative percentages in total fatty acids (Omega-3% and DHA%), using a multi-ethnic genome-wide association study (N = 136,016). PGS models were validated in 437,803 participants of European (EUR), Central/South Asian (CSA), African, and East Asian genetic ancestries. Linear models tested PGS-by-FOS interactions on corresponding observed circulating concentrations. Discovery analysis was performed separately in 237,380 EUR participants and each non-EUR group. Replication analyses were performed using two secondary exposures (i.e., oily fish intake and dietary omega-3 intake) and in another 178,935 EUR participants.

RESULTS: In EUR participants, PGS explained 5.3-11.1% of the phenotypic variance, and significant PGS-by-FOS interactions were detected across all four circulating omega-3 traits. Among participants in the bottom 5% of the PGS distribution, FOS was significantly associated with a 0.40 SD (95% CI: 0.39-0.44) increase in Omega-3. This association effect was 11.1% larger than the population average (β = 0.36; 95% CI: 0.35-0.37; PInt = 0.016) and 42.8% larger than that in participants in the top 5% of the PGS distribution (β = 0.28 SD; 95% CI: 0.25-0.32; PInt = 4.03 × 10[-10]). These interaction patterns were consistently observed in the CSA ancestry and confirmed in replication and sensitivity analyses.

CONCLUSIONS: PGS modify the associations of FOS with circulating omega-3 fatty acids in EUR and CSA populations, with larger FOS effects in participants with lower PGS. These findings support the development of genome-informed precision nutrition.},
}

@article {pmid42709878,
year = {2026},
author = {McGargill, MA and Liu, BC and Kuhns, MS and Mucida, D and Rauch, I and Rodda, LB and Koch, MA and Gonzalez Velozo, H and Cadwell, K and Freedman, TS and Scharschmidt, TC and Sever, R and Ordovas-Montanes, J and Suliman, S and Oberst, A and Runnette, B and Krummel, MF},
title = {Discovery Stack Pilot demonstrates the feasibility and outcomes of a scientist-designed peer-review model that separates quality and impact.},
journal = {PLoS biology},
volume = {24},
number = {9},
pages = {e3003986},
doi = {10.1371/journal.pbio.3003986},
pmid = {42709878},
issn = {1545-7885},
abstract = {Peer review serves as the cornerstone of scientific quality control. Yet, the current journal-centric system is hindered by long timelines, high publication costs, inconsistent review quality, systemic biases, and editorial gatekeeping. Notably, the system relies on misaligned measures of impact that are tethered to journal branding and conflate scientific rigor (Quality) with perceived significance (Impact). Here, we report findings from the Discovery Stack Pilot Study, which tested a scientist-designed, journal-independent peer review model. The Discovery Stack model integrates in-line reviewer comments to promote constructive feedback and separately evaluates scientific Quality and Impact using defined criteria. To examine feasibility and effectiveness, manuscripts were reviewed in parallel with traditional journal review. A total of 162 reviews were completed, and survey data from 86 participants were analyzed. The results showed that reviewers effectively evaluated Quality and Impact as separate dimensions, with Quality scores being more consistent across reviewers than Impact scores. Participants strongly supported the core elements of the Discovery Stack model and expressed enthusiasm for its broader adoption to enhance transparency, efficiency, and value in peer review. Future studies will explore integrating this model into a digital platform for reviewing and curating scientific discoveries to improve the production and dissemination of high-quality research.},
}

@article {pmid42710480,
year = {2026},
author = {Gulleen, EA and Mbarusha, I and Mubiru, D and Pedun, B and Lubwama, M and Niyonzima, N and Sekyanzi, S and Omoding, A and Moore, CC and Phipps, W and Rajasingham, R},
title = {Cost-Effective Diagnostic Algorithms for Ugandan Patients with Solid Tumors Who Develop Chemotherapy-Associated Febrile Illness.},
journal = {The American journal of tropical medicine and hygiene},
volume = {},
number = {},
pages = {},
doi = {10.4269/ajtmh.26-0069},
pmid = {42710480},
issn = {1476-1645},
abstract = {In low- and middle-income settings, microbiologic evaluation of chemotherapy-associated febrile illness is limited by cost. Cost-effective diagnostic algorithms could streamline evaluation for chemotherapy-associated febrile illness where comprehensive testing is not possible, particularly in HIV- and tuberculosis (TB)-endemic settings. In this study, we created a decision analytic model to evaluate costs, diagnostic yield, and cost-effectiveness of diagnostic algorithms for adult inpatients with solid tumors who developed chemotherapy-associated febrile illness in Uganda. Given the high prevalence of HIV, TB, and malaria, diagnostics included serum cryptococcal antigen (CrAg) lateral flow assay, Alere TB urinary lipoarabinomannan (LAM), malaria rapid testing, and aerobic blood cultures. We considered the following testing algorithms: 1) a comprehensive approach where all tests were performed on all participants and 2) stepwise algorithms where tests were performed in series and stopped with the first positive result. Prevalence data and test performance were taken from the published literature. A comprehensive testing strategy yielded 32.2% correct diagnoses at a cost of $97.85 per correct diagnosis. Of the stepwise strategies, testing CrAg first yielded the cheapest strategy at a cost of $85.49 per correct diagnosis and the highest number of appropriate diagnoses (29.9%). The incremental cost-effectiveness ratio was $234 per additional correct diagnosis for the comprehensive strategy when compared with the sequential strategy. Although comprehensive diagnostic testing is optimal for patients who experience chemotherapy-associated febrile illness, if this strategy is unavailable, stepwise testing with CrAg first and then, TB LAM is optimal to maximize correct diagnosis and minimize costs.},
}

@article {pmid42711241,
year = {2026},
author = {Perales, MA and Dietrich, J and Gust, J and Santomasso, B and Rejeski, K and Hansen, D and Shah, NN and Berdeja, J and Bishop, M and Bleickardt, E and Brudno, J and Dahiya, S and Frey, N and Frigault, MJ and Gardner, R and Ghobadi, A and Grupp, S and Hamadani, M and Jacobson, C and Jain, MD and Jain, T and Komanduri, KV and Kumar, A and Lim, S and Lin, Y and Miao, H and Neelapu, S and Otegbeye, F and Park, JH and Pasquini, M and Patel, N and Plautz, G and Verdun, N and Lee, DW and Maus, MV and Locke, FL},
title = {ASTCT Consensus Grading for Toxicities after Immune Effector Cell Therapy.},
journal = {Transplantation and cellular therapy},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.jtct.2026.05.020},
pmid = {42711241},
issn = {2666-6367},
abstract = {In 2019, the American Society for Transplantation and Cellular Therapy (ASTCT) developed consensus definitions and grading criteria for the common immune effector cell (IEC)-associated toxicities of cytokine release syndrome (CRS) and IEC-associated neurotoxicity syndrome (ICANS). These grading scales were widely adopted by clinicians, investigators, and sponsors, allowing a clearer understanding of outcomes across clinical trials and a uniform basis to inform treatment algorithms. Since then, other IEC class effects, such as IEC-associated hemophagocytic lymphohistiocytosis-like syndrome (IEC-HS) and non-ICANS attributable neurotoxicity, have been recognized. ASTCT convened experts for 2 tasks. First, to consider updating the previously published ASTCT grading criteria for CRS, ICANS, and IEC-HS. Second, to consider existing definitions and grading criteria, and/or create consensus criteria for emerging toxicities, including immune effector cell-associated hematotoxicity; non-ICANS neurological toxicities such as parkinsonism, cranial nerve palsies, and polyneuropathies; IEC-associated enterocolitis; tumor inflammation-associated neurotoxicity; and on-target, off-tumor toxicities. These updated consensus toxicity definitions and grading criteria can facilitate comparisons of toxicities of IEC and T-cell engager therapy across clinical trials and in real-world settings, as well as aid clinicians in better characterizing the severity of toxicity that can ultimately be tied to management guidelines.},
}

@article {pmid42714438,
year = {2026},
author = {Farhadi, F and Rajagopal, JR and Ide Bolet, S and Dutta, J and Catalano, OA and Iravani, A and Esfahani, SA and Jadvar, H and Heidari, P},
title = {Artificial Intelligence Across the PET Reconstruction Pipeline: An Update.},
journal = {AJR. American journal of roentgenology},
volume = {},
number = {},
pages = {},
doi = {10.2214/AJR.26.34681},
pmid = {42714438},
issn = {1546-3141},
abstract = {PET reconstruction has evolved from analytic and iterative physics-based methods toward hybrid approaches that increasingly incorporate artificial intelligence (AI). As digital detectors, long-axial FOV systems, and time-of-flight technology increase data richness and computational demand, AI, particularly deep learning, is being used across the acquisition, correction, reconstruction, and postprocessing stages to stabilize low-count imaging, refine system modeling, and improve noise-resolution tradeoffs while preserving clinically relevant image interpretation. In this context, most AI methods function to augment-rather than replace-established physics-based reconstruction frameworks. Early clinical and multicenter studies have demonstrated that selected AI-based methods maintain noninferior diagnostic performance and key quantitative metrics within defined acquisition and reconstruction contexts. As these tools transition from research into routine practice, their implementation is shaped by intended-use validation, interoperability, traceability, and software lifecycle management requirements. This Review explores the application of AI across the PET reconstruction pipeline, discussing technical foundations, highlighting key clinical implications, and considering regulatory and other practical issues that govern safe and reproducible deployment. Reconstruction pipeline steps considered in the article include mathematical inversion of projection data into images, signal processing during acquisition, prereconstruction corrections, system modeling incorporated into reconstruction, and postreconstruction processing steps that directly influence reconstructed image properties.},
}

@article {pmid42714969,
year = {2026},
author = {Levi, A and Nasr, A and Cui, Y and Abbas, AA and Arouchian, TT and Coveler, AL and Pierce, TL and Anderson, BT and Collisson, E and Davelaar, J and Lo, SK and Gaddam, S and Gong, J and Osipov, A and Hendifar, AE},
title = {Young Women With Pancreatic Cancer: A High-Risk Group for Demoralization.},
journal = {Psycho-oncology},
volume = {35},
number = {9},
pages = {e70601},
pmid = {42714969},
issn = {1099-1611},
mesh = {Humans ; Female ; *Pancreatic Neoplasms/psychology ; *Depression/psychology ; Aged ; Middle Aged ; *Demoralization ; *Adaptation, Psychological ; Risk Factors ; *Stress, Psychological/psychology ; Male ; Aged, 80 and over ; Surveys and Questionnaires ; },
abstract = {BACKGROUND: Demoralization is a maladaptive coping response to stressful situations, characterized by thoughts of hopelessness, helplessness, and loss of meaning and purpose. Demoralization is clinically measurable using the Demoralization Scale 2 (DS-II). Pancreatic cancer (PC) patients, who carry a notoriously poor prognosis, are hypothesized to be at higher risk of demoralization.

AIMS: This study uses the DS-II to gauge the impact of demoralization in PC patients compared to a heterogenous cancer population and establish its relation to depression.

METHODS: Patients completed the DS-II, PHQ-9, and a demographic survey. The mean DS-II score of PC patients was compared with that of a previously published heterogenous cancer cohort reported by Ignatius et al. using a one-sample t-test. The univariable association between DS-II scores and PHQ-9 scores was examined using linear regression models.

RESULTS: Of the 206 patients enrolled in the study, 47% were women and the mean age was 67 ± 10 years. The mean DS-II total score was 4.9 ± 5.2 points, significantly lower than the mean of 10.8 ± 8.0 previously reported by Ignatius and De La Garza II in a psychiatric oncology cohort (p < 0.001). There was no significant difference in demoralization scores across disease stages (p = 0.8). DS-II scores in univariable models were associated with depression (β = 0.79, p < 0.001), age (β = -0.09, p = 0.008), and women (p = 0.002).

CONCLUSION: Demoralization in this cohort of patients with PC was lower than that reported by Ignatius et al., although differences in recruitment settings and patient characteristics limit direct comparisons. Though disease stage did not impact demoralization scores in PC, our study found demoralization was strongly associated with concurrent depression, young age, and women. Understanding the risk factors associated with demoralization in PC can help enhance the quality of psychosocial care in oncology.},
}

Humans
Female
*Pancreatic Neoplasms/psychology
*Depression/psychology
Aged
Middle Aged
*Demoralization
*Adaptation, Psychological
Risk Factors
*Stress, Psychological/psychology
Male
Aged, 80 and over
Surveys and Questionnaires

@article {pmid42705894,
year = {2026},
author = {Dimitrov, D and Matrajt, L and Ren, X and Stansfield, SE and Moore, M},
title = {Why accurate risk stratification matters in HIV population modeling.},
journal = {Mathematical biosciences and engineering : MBE},
volume = {23},
number = {8},
pages = {2307-2322},
doi = {10.3934/mbe.2026084},
pmid = {42705894},
issn = {1551-0018},
mesh = {Humans ; *HIV Infections/epidemiology/transmission ; Incidence ; Computer Simulation ; Disease Progression ; Risk Assessment ; Epidemics ; Risk Factors ; Epidemiological Models ; Models, Biological ; Algorithms ; },
abstract = {Accurate representation of behavioral risk heterogeneity significantly influences the projections of Human Immunodeficiency Virus transmission models without receiving the deserved attention when models are structured. As a result, models widely vary in how they stratify risk and how individuals progress through risk groups. We systematically evaluated how these two structural features-the number of risk groups and assumptions about risk progression (comparing three mechanisms of fixed, age-based, or mixed risk)-shape epidemic projections. Using deterministic HIV models stratified by HIV stage and behavioral risk, we simulated populations over 250 years under standardized initial conditions. Our results show that risk-progression mechanisms strongly influence long-term epidemic behavior. Fixed-risk models gradually shift the population toward lower-risk groups, thus reducing HIV incidence over time. In contrast, age-based progression sustains a larger high-risk population and produces a substantially higher long-term incidence, while mixed progression yields intermediate outcomes. The granularity of risk stratification further modifies the projections: models with more risk groups generate significantly different incidence trajectories and equilibrium population sizes under age-based and mixed progression, whereas fixed-risk models produce similar long-term results with a different number of risk groups. These findings highlight that both risk-progression assumptions and the level of stratification can meaningfully alter HIV forecasts. Therefore, the careful treatment of population risk heterogeneity is essential to generate reliable projections and to guide intervention strategies.},
}

Humans
*HIV Infections/epidemiology/transmission
Incidence
Computer Simulation
Disease Progression
Risk Assessment
Epidemics
Risk Factors
Epidemiological Models
Models, Biological
Algorithms

@article {pmid42706231,
year = {2026},
author = {Prokunina-Olsson, L and Florez-Vargas, O and Levin, MG and Dutta, D and Breeze, CE and Hurwitz, LM and Yan, W and Lamy, P and Papenberg, BW and Wang, K and Lee, CH and Milne, RL and Gu, J and Um, CY and Joseph, V and Furberg, H and Le Calvez-Kelm, F and Lori, A and Choudhury, PP and Afshar, N and Kogevinas, M and Offit, K and Vermeulen, SH and López de Maturana, E and Albanes, D and Purdue, MP and Cortessis, VK and Karagas, MR and Kooperberg, C and Bjurlin, M and Tadesse, DA and Moore, SC and Huang, WY and Haiman, CA and Stern, MC and Eliassen, AH and Mucci, LA and Aben, KK and Galesloot, TE and , and Verma, A and Yoshino, S and Hikino, K and Terao, C and Rafnar, T and Matsuda, K and Shuin, T and Garcia-Closas, M and Real, FX and Kiemeney, LA and Chanock, SJ and Malats, N and Silverman, DT and Dyrskjot, L and Rothman, N and Damrauer, SM and Koutros, S and Damrauer, JS},
title = {Multi-population GWAS meta-analysis identifies bladder cancer susceptibility loci and highlights genetic regulation of smoking-related risk.},
journal = {Nature communications},
volume = {17},
number = {1},
pages = {},
pmid = {42706231},
issn = {2041-1723},
support = {2023-0224//Doris Duke Charitable Foundation (DDCF)/ ; },
mesh = {Humans ; *Urinary Bladder Neoplasms/genetics ; Genome-Wide Association Study ; *Genetic Predisposition to Disease ; *Smoking/genetics/adverse effects ; Polymorphism, Single Nucleotide ; Genetic Risk Score ; Gene Expression Regulation, Neoplastic ; Receptors, Nicotinic/genetics/metabolism ; Risk Factors ; Chromosomes, Human, Pair 15/genetics ; Genetic Loci ; },
abstract = {Bladder cancer is the ninth most common cancer worldwide, caused by genetic and environmental risk factors. Here, we report the findings of a multi-population meta-analysis of genome-wide association studies, including 32,470 individuals with and 1,753,462 without bladder cancer. We identify 70 independent risk loci, of which 43 are novel. Using a 70-marker polygenic risk score (HR = 1.63 per standard deviation), we increase the area under the curve from 0.71 (baseline risk model) to 0.75. Integrative analyses reveal the enrichment of the associated variants within accessible chromatin regions, and of the prioritized genes within pathways for xenobiotic metabolism and smoking behavior. Specifically, we show that the 15q25.1 variant rs71581744-ACCCC/A co-localizes with tissue-specific CHRNA3 expression, modulates mRNA stability, and associates with risk of muscle-invasive bladder cancer among current smokers. Together, these findings substantially expand the known genetic architecture of bladder cancer risk and highlight the germline regulation of smoking behavior as a mechanism driving bladder cancer susceptibility.},
}

Humans
*Urinary Bladder Neoplasms/genetics
Genome-Wide Association Study
*Genetic Predisposition to Disease
*Smoking/genetics/adverse effects
Polymorphism, Single Nucleotide
Genetic Risk Score
Gene Expression Regulation, Neoplastic
Receptors, Nicotinic/genetics/metabolism
Risk Factors
Chromosomes, Human, Pair 15/genetics
Genetic Loci

@article {pmid42706341,
year = {2026},
author = {Diehl, MI and Basto, PA and Abikenari, MA and Linde, IL and Okwan-Duodu, D and Engleman, EG},
title = {Neutrophils in cancer.},
journal = {Nature reviews. Cancer},
volume = {},
number = {},
pages = {},
pmid = {42706341},
issn = {1474-1768},
abstract = {Neutrophils, long appreciated for their central role in host defences, have largely pro-tumorigenic effects in cancer owing to their sensitivity to signals in the tumour environment. Cancers regularly co-opt the functions of neutrophils to promote angiogenesis, immunosuppression, tumour growth and metastasis. However, depending on context, many of the same neutrophil-derived factors involved in these processes can mediate tumour cell killing. In this Review, we examine the functions of neutrophils and their impact on cancer, drawing parallels between their roles in cancer and non-cancer contexts, and highlighting their remarkable sensitivity to environmental cues. We call attention to promising strategies for targeting and manipulating neutrophils for the treatment of cancer.},
}

@article {pmid42706837,
year = {2026},
author = {Ueha, S and Aoki, H and Takahashi, M and Shichino, S and Matsushima, K},
title = {Spatiotemporal CD8[+] T-Cell Dynamics: Clonal Replacement and Expansion as Determinants of Sustainable Antitumor Response.},
journal = {Cancer science},
volume = {},
number = {},
pages = {},
pmid = {42706837},
issn = {1349-7006},
support = {20H03474//Japan Society for the Promotion of Science/ ; 23K27397//Japan Society for the Promotion of Science/ ; JP22ama221306//Japan Agency for Medical Research and Development/ ; JP22fk0310509//Japan Agency for Medical Research and Development/ ; JP25fk0310531//Japan Agency for Medical Research and Development/ ; JP26ck0106121//Japan Agency for Medical Research and Development/ ; },
abstract = {The clinical success of immune checkpoint inhibitors (ICI) has shifted the paradigm of cancer treatment, yet the fundamental mechanisms governing the long-term sustainability of antitumor T-cell responses remain elusive. Emerging evidence suggests that the efficacy of ICI depends not only on the reinvigoration of pre-existing tumor-infiltrating lymphocytes but also on the continuous mobilization and replacement of T-cell clones from systemic reservoirs. In this review, we propose a "spatiotemporal ecosystem model" of the antitumor T-cell response. We first delineate the spatial dynamics of T-cell clones, where tumor-reactive progenitors primed in the tumor-draining lymph nodes (dLN) circulate through the peripheral blood to replenish the tumor microenvironment (TME). We highlight that TCR avidity emerges as a key determinant of clonal fate; while high-avidity clones provide potent early cytotoxicity, their susceptibility to accelerated terminal exhaustion eventually creates an available niche that allows for the subsequent expansion of intermediate-avidity successor clones. Furthermore, we discuss how single-cell multi-omics integration (transcriptome, TCR repertoire, and epigenome) reveals that clonal fate is functionally encoded in the molecular and metabolic poise of T cells prior to their expansion. Finally, we discuss the potential of monitoring these clonal dynamics through liquid biopsy as a non-invasive window into the resilience of the immune ecosystem, distinguishing responders with sustainable, polyclonal mobilization from non-responders with frustrated, oligoclonal responses. By integrating clonal evolution, metabolic fitness, and inter-organ crosstalk, this ecosystem perspective offers a comprehensive framework for predicting therapeutic outcomes and developing next-generation precision immunotherapies.},
}

@article {pmid42707015,
year = {2026},
author = {Park, JJS and Nayudu, K and Raymundo, C and Olsen, E and Kim, E and Mehta-Shah, N and Ottevanger, R and Thornton, S and Scarisbrick, J and Perez-Chada, L and Larocca, C and Shinohara, MM},
title = {Qualitative assessment of the content validity of pruritus patient-reported outcome measures in mycosis fungoides and Sézary syndrome.},
journal = {The British journal of dermatology},
volume = {},
number = {},
pages = {},
doi = {10.1093/bjd/ljag379},
pmid = {42707015},
issn = {1365-2133},
}

@article {pmid42708362,
year = {2026},
author = {Gertych, A and Ye, H and Chen, X and Vail, E and Ramanujan, VK and Brady, L and True, LD and Nelson, PS and Carroll, PR and Theodorescu, D},
title = {Human Y chromosome pan-organ mapping reveals progressive mosaic loss from normal to cancer.},
journal = {JCI insight},
volume = {11},
number = {17},
pages = {},
pmid = {42708362},
issn = {2379-3708},
support = {P01 CA163227/CA/NCI NIH HHS/United States ; P50 CA097186/CA/NCI NIH HHS/United States ; R35 CA294022/CA/NCI NIH HHS/United States ; },
mesh = {Humans ; Male ; *Chromosomes, Human, Y/genetics ; *Mosaicism ; In Situ Hybridization, Fluorescence ; *Neoplasms/genetics/pathology ; },
abstract = {BACKGROUND: Loss of the Y chromosome (LOY) is a frequent event in male tumors and has been linked to cancer progression. However, the degree of mosaic LOY (mLOY) within normal tissues from men with or without cancer remains uncharacterized.

METHODS: Here we used a FISH-based assay targeting X- and Y-chromosome centromeres to perform a pan-organ analysis of mLOY in 1,000 male tissue samples from 405 individuals representing 11 organs. Automated image processing generated a quantitative FISH-based mLOY score (YchrFISH) that we validated against a transcriptomic surrogate of Y-chromosome dosage from RNA-seq data.

RESULTS: mLOY burden varied by tumor type, with highest degree in colorectal carcinoma. Across tissue groups, YchrFISH scores declined progressively from normal tissues of cancer-free men to histologically normal tissues adjacent to cancer and carcinoma (P < 0.0001). Paired analyses confirmed consistently greater mLOY in malignant compared with tumor-adjacent histologically normal tissue in different organs. Spatially resolved RNA-seq maps of bladders removed for cancer demonstrated a transcriptional gradient of Y-chromosome loss from normal urothelium through intraepithelial neoplasia to invasive carcinoma.

CONCLUSION: mLOY gradients exist across histologically normal and malignant tissues, consistent with the concept of field cancerization. Our findings support epithelial mLOY as a biomarker of early malignant transformation and, to our knowledge, a previously unrecognized hallmark of male oncogenesis.

FUNDING: NIH grants R35CA294022, P01CA163227, and P50CA97186 (the Pacific Northwest Prostate Cancer SPORE) and the Institute for Prostate Cancer Research.},
}

Humans
Male
*Chromosomes, Human, Y/genetics
*Mosaicism
In Situ Hybridization, Fluorescence
*Neoplasms/genetics/pathology

@article {pmid42708883,
year = {2026},
author = {Bai, H and Juraska, M and Magaret, CA and Yssel, A and Rossenkhan, R and Murrell, B and Dearlove, BL and Lewitus, E and deCamp, AC and Giorgi, EE and Ludwig, J and Westfall, DH and Deng, W and Chen, L and Zhao, H and Pankow, A and Bhattacharya, T and York, T and Gwashu-Nyangiwe, A and Ndabambi, N and Thebus, R and Ake, JA and Vasan, S and Randhawa, A and Hural, JA and Edupuganti, S and Mgodi, N and Karuna, ST and Morris, L and Montefiori, DC and Cohen, MS and Corey, L and Edlefsen, PT and McElrath, MJ and Gilbert, PB and Williamson, C and Mullins, JI and Rolland, M},
title = {VRC01 exerted differential pressure on HIV-1 Env from subtypes B and C that continued in the first weeks post-diagnosis in the AMP trials.},
journal = {The Journal of infectious diseases},
volume = {},
number = {},
pages = {},
doi = {10.1093/infdis/jiag454},
pmid = {42708883},
issn = {1537-6613},
abstract = {BACKGROUND: The Antibody Mediated Prevention trials (HVTN 703 and HVTN 704) demonstrated that infusions of the bnAb VRC01 prevented HIV-1 acquisition with viruses sensitive to VRC01 neutralization. We evaluated how VRC01 epitope distances differed across groups in the trials.

METHODS: We calculated VRC01 epitope distances (a 3D structure informed measure of how the VRC01 epitope in a sequence differs from that epitope in known VRC01 sensitive strains) to compare >35,000 Envelopes sampled from 172 participants with mostly subtype C viruses in HVTN 703 and subtype B in HVTN 704.

RESULTS: At the first visit with detectable HIV-1, we found fewer distinct VRC01 epitopes in the sequences from participants in the VRC01 high-dose group in HVTN 704 (p=0.054), suggesting that some epitope variants were blocked in these participants who harbored subtype B viruses. In both trials, VRC01 epitope distances were significantly larger in the VRC01 high-dose groups than in the placebo groups (p≤0.010). Moreover, sequences sampled in the first month after diagnosis showed that the rate of change in VRC01 epitope distances was significantly higher in the VRC01 groups than in the placebo in the HVTN 703 trial (p≤0.036).

CONCLUSIONS: These findings show the impact of sieve acquisition (variants blocked among subtype B viruses) and post-acquisition (stronger impact of VRC01-mediated escape in subtype C) effects, highlighting a complex intersection between HIV-1 subtypes, escape pathways and antibody-mediated prevention. The differential pressure exerted by VRC01 on subtype B vs. C viruses emphasizes that escape pathways need to be considered when selecting bnAbs for clinical trials.},
}

@article {pmid42709436,
year = {2026},
author = {Zheng, DJ and Oranges, K and Ramakrishnan, S and Ji, L and Beauchemin, MP and Alexander, SW and Leahy, AB and Bona, K and Caywood, EH and Castellino, SM and Gupta, S and Hawkins, DS and Militano, O and Montgomery, KE and Newman, H and Rau, RE and Rheingold, S and Robles, JM and Roth, ME and Teachey, D and Vargas, S and Zupanec, S and Parsons, SK},
title = {Blinatumomab Care Delivery for Pediatric B-Cell Acute Lymphoblastic Leukemia.},
journal = {JAMA network open},
volume = {9},
number = {9},
pages = {e2632786},
pmid = {42709436},
issn = {2574-3805},
support = {U10 CA180899/CA/NCI NIH HHS/United States ; },
mesh = {Humans ; *Antibodies, Bispecific/therapeutic use ; United States ; Child ; Female ; Male ; *Precursor B-Cell Lymphoblastic Leukemia-Lymphoma/drug therapy ; *Antineoplastic Agents/therapeutic use ; Child, Preschool ; *Delivery of Health Care ; Adolescent ; Infant ; },
abstract = {IMPORTANCE: Blinatumomab, a novel immunotherapy administered as a 28-day continuous infusion, has fundamentally shifted the treatment paradigm for pediatric B-cell acute lymphoblastic leukemia (B-ALL) and is now considered a component of standard therapy for the most common childhood cancer. However, the care delivery challenges in transitioning from an experimental agent on a clinical trial to widespread clinical implementation are unknown.

OBJECTIVE: To characterize the clinical landscape of pediatric blinatumomab care-delivery practice and challenges in the US from the perspective of treating centers.

This survey study was conducted from February to March 2025 among US member institutions of the Children's Oncology Group (COG) across 44 states.

EXPOSURE: Institutional characteristics, including participation in the National Cancer Institute Community Oncology Research Program (NCORP), US census region, site-reported annual pediatric ALL patient volume, and prior blinatumomab experience, were assessed.

MAIN OUTCOMES AND MEASURES: Incorporation of blinatumomab as standard therapy by pediatric B-ALL subtype; major outpatient care-delivery challenges defined as 4 or 5 on a 5-point Likert scale by more than 25% of centers.

RESULTS: Of 195 active US COG member institutions, 147 centers completed the survey and were successfully matched with a unique COG identifier, among which 35 institutions (23.8%) were NCORP participants. There were 32 institutions (21.8%) in Midwest, 30 institutions (20.4%) in Northeast, 60 institutions (40.8%) in South, and 25 institutions (17.0%) in West census regions. Most centers reported using blinatumomab as their institutional standard therapy for National Cancer Institute standard risk-average (134 centers [91.2%]), standard risk-high (144 centers [98.0%]), and high-risk (140 centers [95.2%]) B-ALL. Fewer centers reported using blinatumomab for infant (83 centers [56.5%]) or Philadelphia chromosome-positive (96 centers [65.3%]) B-ALL. The most common major outpatient blinatumomab site care-delivery challenges included lack of home care companies (75 centers [51.0%]), family distance to treating center (41 centers [27.9%]), and insurance coverage for home care companies (37 centers [25.2%]). There were 67 sites (45.6%) that reported having no home care company options for any patients.

CONCLUSIONS AND RELEVANCE: In this study, challenges associated with pediatric blinatumomab home care were highly prevalent, with broader implications for health system infrastructure availability. These data highlight a need to plan for clinical implementation strategies alongside the development and testing of novel therapies.},
}

Humans
*Antibodies, Bispecific/therapeutic use
United States
Child
Female
Male
*Precursor B-Cell Lymphoblastic Leukemia-Lymphoma/drug therapy
*Antineoplastic Agents/therapeutic use
Child, Preschool
*Delivery of Health Care
Adolescent
Infant

@article {pmid42702625,
year = {2026},
author = {Weidle, C and Brunette, N and Wrenn, SP and Fiala, B and Ravichandran, R and Carr, KD and Zak, SE and Zumbrun, EE and Bakken, RR and Murphy, M and Peng, Z and Chan, S and Skotheim, R and Carter, L and Correnti, CE and Dye, JM and Baker, D and King, NP and Borst, AJ and Stewart, LJ},
title = {Pan-Ebolavirus nanoparticle vaccine provides protection in rodents from lethal infection by Zaire and Sudan viruses.},
journal = {Nature communications},
volume = {17},
number = {1},
pages = {},
pmid = {42702625},
issn = {2041-1723},
support = {HDTRA1-18-1-0001//United States Department of Defense | Defense Threat Reduction Agency (DTRA)/ ; },
mesh = {Animals ; *Hemorrhagic Fever, Ebola/prevention & control/immunology/virology ; Guinea Pigs ; *Ebolavirus/immunology ; Mice ; Antibodies, Viral/immunology ; Nanovaccines ; *Ebola Vaccines/immunology/administration & dosage ; *Nanoparticles/chemistry ; Antibodies, Neutralizing/immunology ; Female ; Glycoproteins/immunology ; Disease Models, Animal ; Humans ; Mice, Inbred BALB C ; },
abstract = {Both Zaire ebolavirus (EBOV) and Sudan ebolavirus (SUDV) are members of the genus Ebolavirus and cause outbreaks marked by high fatality rates and repeated spillover from animal reservoirs. Filoviral glycoproteins (GPs) are the primary targets of neutralizing antibodies and form the basis of current vaccines. Here we describe the design, structural characterization, and evaluation of two-component self-assembling icosahedral I53-50 nanoparticles displaying prefusion EBOV or SUDV GP antigens, either individually or in cocktail and mosaic multivalent formats. EBOV-GP-I53-50 and SUDV-GP-I53-50 nanoparticles elicited strong homologous protection in mice and guinea pigs. In the mouse-adapted EBOV model (maEBOV), mosaic and cocktail formulations produced weak survival below that of the matched EBOV-GP-I53-50 GP immunogen. In contrast, in the gpaSUDV guinea pig model (gpSUDV), cocktail and mosaic nanoparticles elicited robust protection against gpSUDV, and detectable antibody responses to both SUDV and EBOV GPs. These findings demonstrate that multivalent GP-I53-50 nanoparticle immunogens can protect rodents from death, severe clinical signs of disease, and weight loss in relevant models. Together with the established clinical safety of the I53-50 platform, these results support continued efforts toward the development of a pan-ebolavirus vaccine.},
}

Animals
*Hemorrhagic Fever, Ebola/prevention & control/immunology/virology
Guinea Pigs
*Ebolavirus/immunology
Mice
Antibodies, Viral/immunology
Nanovaccines
*Ebola Vaccines/immunology/administration & dosage
*Nanoparticles/chemistry
Antibodies, Neutralizing/immunology
Female
Glycoproteins/immunology
Disease Models, Animal
Humans
Mice, Inbred BALB C

@article {pmid42705169,
year = {2026},
author = {Kalyanasundaram, A and Kifle, DW and Davis, J and Balkhi, MY and Arya, A and Mayer, BT and Lemire, G and Krishnappa, D and Siribie, M and Jeon, H and Tadesse, BT and Rakotozandrindrainy, N and Razafimanantsoa, R and Noellie, HB and Ouedraogo, NI and Diarra, A and Velavan, TP and Gray, SA and Lee, J and Rakotozandrindrainy, R and Sirima, SB and Jackson, LA and Marks, F and Carter, D and Siddiqui, AA},
title = {Antibody-mediated functional responses induced by the SchistoShield® schistosomiasis vaccine in disease-naïve and endemic human populations.},
journal = {Vaccine},
volume = {92},
number = {},
pages = {129129},
doi = {10.1016/j.vaccine.2026.129129},
pmid = {42705169},
issn = {1873-2518},
abstract = {Schistosomiasis (bilharzia) is a neglected tropical disease caused by Schistosoma spp. Clinical manifestation of chronic schistosomiasis include but not restricted to anemia, growth stunting, hepatosplenomegaly, cognitive impairment in children and male/female genital schistosomiasis. Praziquantel (PZQ) remains the principal standard treatment for schistosomiasis, but concerns about its reduced effectiveness against larval stages, reinfections, and emerging drug resistance reinforces the urgent need for a vaccine. SchistoShield®, composed of Sm-p80 antigen with GLA-SE adjuvant, is a promising vaccine candidate that has successfully completed phase 1 and 1b clinical trials in the USA and two countries in Africa (Madagascar and Burkina Faso). In this study, SchistoShield® vaccine specific total IgG antibody titers were measured from serum samples collected at multiple time points from both the USA and Africa trials. Results demonstrate that total IgG titers increased at week 5 after the first booster and peaked at weeks 9 and 12. Furthermore, in vitro schistosomula killing assays and heterologous passive transfer of purified total IgG in mice were performed to evaluate the role of vaccine-induced antibodies against schistosomes. Sera collected from individuals enrolled in the USA, Burkina Faso, and Madagascar trials, exhibited 69.2%, 55.1%, and 34.3% in vitro schistosomula killing, respectively, indicative of potent anti-worm antibody responses. Passive transfer of human total IgG from vaccinated individuals in mice revealed notable reductions in worm burden, egg counts, and egg-hatching ability compared to groups given pre-vaccination sera across all trials. Overall, these findings support that SchistoShield® induces generation of functional antibodies that may play a crucial role in antibody-mediated protection against schistosomiasis.},
}

@article {pmid42006783,
year = {2026},
author = {Zheng, J and Steinfelder, RS and Yin, H and Qu, C and Thomas, M and Thomas, SS and Andrews, C and Augusto, B and Corley, DC and Lee, JK and Berndt, SI and Chan, AT and Chanock, SJ and Gignoux, C and Goldberg, SR and Haiman, CA and Huyghe, JR and Iwasaki, M and Marchand, LL and Lee, SC and Melendez, J and Mesa, I and Ogino, S and Sifontes, V and Um, CY and Visvanathan, K and White, LL and Williams, A and Willis, W and Wolk, A and Yamaji, T and Vadaparampil, ST and Jarvik, GP and Burnett-Hartman, AN and Milne, RL and Platz, EA and Figueiredo, JC and Zheng, W and MacInnis, RJ and Palmer, JR and Schmit, SL and Landorp-Vogelaar, I and Peters, U and Hsu, L},
title = {MyGeneRisk Colon: A Web-Based Tool for Personalized Colorectal Cancer Risk Prediction Based on Genetics and Lifestyle.},
journal = {medRxiv : the preprint server for health sciences},
volume = {},
number = {},
pages = {},
pmid = {42006783},
abstract = {Colorectal cancer (CRC) is a leading cause of cancer-related death, with incidence rising substantially among individuals under 50 years of age. Polygenic risk scores (PRS) hold promise for identifying high-risk individuals; when combined with lifestyle factors, they substantially improve prediction accuracy compared with models based on lifestyle factors alone. However, few clinical tools currently exist that facilitate this integrated, PRS-enhanced risk assessment. To bridge this gap, we developed MyGeneRisk Colo n, a publicly accessible web portal that delivers individualized CRC risk prediction by incorporating genetic, demographic, family history, and lifestyle factors. This paper details the development of the underlying risk prediction model, the portal's architecture and data security, our reporting framework, and engagement with a community advisory panel. Designed as a user-friendly platform, MyGeneRisk Colon aims to effectively communicate personalized CRC risk profiles and educate users and healthcare providers about prevention strategies.},
}

@article {pmid42701054,
year = {2026},
author = {Garcia-Gonzalez, P and Forsyth, C and Herzog, L and Annamalay, A and Radich, J},
title = {Chronic Myeloid Leukemia in Low- and Middle-Income Countries: Increasing Access to Tyrosine Kinase Inhibitors and Supporting Treatment-Free Remission.},
journal = {Clinical lymphoma, myeloma & leukemia},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.clml.2026.08.003},
pmid = {42701054},
issn = {2152-2669},
abstract = {Chronic myeloid leukemia (CML) is a leading example of how targeted therapy can transform cancer outcomes. Since the introduction of tyrosine kinase inhibitors (TKIs), survival in high-income countries has approached that of the general population. Large-scale access initiatives have demonstrated that sustained delivery of TKIs is also feasible in low- and middle-income countries (LMICs), with comparable outcomes, challenging assumptions about the limits of cancer care in resource-constrained settings. As treatment access has expanded in LMICs, the central challenge in CML care has shifted to delivery of optimized, sustainable care. Achieving optimal outcomes requires timely diagnosis, sustained adherence, regular molecular monitoring, and the ability to adjust treatment based on individual patients' tolerance and response to therapy. However, gaps in diagnostic capacity, lack of coordination in care delivery, and persistent socioeconomic barriers continue to limit continuity of care and constrain the full benefits of therapy. Here we review the evidence on the evolving landscape of CML care in LMICs, including treatment access, molecular monitoring, adherence, and treatment-free remission (TFR). Molecular monitoring represents the critical bottleneck linking treatment access to optimized care and long-term outcomes, requiring innovative tools and approaches to scale up access to molecular diagnostics in resource-limited settings. Advancing equitable outcomes in CML will require multiple partners, including industry, government, academia, and nonprofit entities. Access barriers for CML are a global concern, and lessons learned in addressing these challenges in LMICs may inform program strategies in other contexts, including marginalized communities in high-income countries.},
}

@article {pmid42702214,
year = {2026},
author = {Daly, ME and Simone, CB and Redman, MW and Hsieh, MH and Hesketh, PJ and Hu, C and Monjazeb, AM and Steuer, CE and Ganti, AK and Kashani, R and Bauman, JR and Feliciano, JL and Moon, J and Ku, K and Le-Lindqwister, N and Baschnagel, AM and Maraboyina, S and Sherwood, GB and Almquist, D and Higgins, KA and Gray, JE and Bradley, JD and Kelly, K},
title = {Induction and consolidation atezolizumab with stereotactic body radiation therapy versus radiation alone in high-risk, early-stage non-small-cell lung cancer (SWOG/NRG S1914): a multicentre, open-label, superiority, phase 3, randomised controlled trial.},
journal = {Lancet (London, England)},
volume = {},
number = {},
pages = {},
doi = {10.1016/S0140-6736(26)01655-7},
pmid = {42702214},
issn = {1474-547X},
support = {U10 CA180822/CA/NCI NIH HHS/United States ; U10 CA180868/CA/NCI NIH HHS/United States ; },
abstract = {BACKGROUND: Stereotactic body radiation therapy (SBRT) is the standard of care for early-stage, medically inoperable non-small-cell lung cancer (NSCLC). We aimed to test the addition of neoadjuvant, concurrent, and adjuvant atezolizumab with SBRT for early-stage NSCLC.

METHODS: In this multicentre, open-label, phase 3, randomised controlled trial, eligible patients from 146 institutions across the USA who had T1-T3N0M0 NSCLC ≤7 cm, and were medically inoperable or declined surgery, and had at least one risk factor suggestive of increased risk of recurrence, were included in the study. Patients underwent open-label equal and stratified randomisation to SBRT over three to eight fractions with or without up to eight cycles of neoadjuvant, concurrent, and adjuvant atezolizumab 1200 mg intravenously every 21 days for up to eight cycles, with SBRT initiated with cycle three. The primary objective was to compare overall survival between the two groups. The group sequential design included four interim analyses. Target accrual was 480 patients (432 eligible). The trial is registered with ClinicalTrials.gov (NCT04214262) and is closed to new participants.

FINDINGS: Between March 25, 2020, and Sept 9, 2024, 417 patients were enrolled and randomly assigned to atezolizumab plus SBRT (n=210) or SBRT alone (n=207). 402 were eligible and made up the modified intention-to-treat population (201 per group). The median age was 72·8 years (IQR 67·4-78·4), 218 (54%) of 402 participants were female, and 184 (46%) were male. Accrual closed at the first interim analysis of all randomly assigned participants for futility with 76 progression-free survival (PFS) events and 41 deaths among 400 eligible participants (200 per group). An updated analysis was performed with 140 PFS events, 92 deaths, and a median of 24·8 months (range 0·1-64·9; IQR 18·6-36·0) of follow-up among living patients. The overall survival hazard ratio was 1·04 (95% CI 0·69-1·58; one-sided p=0·58). Estimated 2-year overall survival was 82% in both groups (95% CI 75-87). Grade 3 or higher adverse event rates were 12% with atezolizumab plus SBRT and 3% with SBRT. Two grade 5 respiratory events occurred in the atezolizumab plus SBRT group.

INTERPRETATION: In the first fully reported phase 3 cooperative group trial to assess immunotherapy in inoperable early-stage NSCLC, we observed no improvement in overall survival with atezolizumab plus SBRT, and more grade 3 or higher adverse events were reported with atezolizumab combined with SBRT.

FUNDING: US National Institutes of Health, US National Cancer Institute, and Genentech.},
}

@article {pmid42428052,
year = {2026},
author = {Plender, EG and Prodanov, T and Lin, J and Wong, I and Wertz, J and Gordon, WW and Bamshad, MJ and Munson, KM and O'Neal, WK and Bloom, JD and , and Marschall, T and Eichler, EE},
title = {Complex structural variation, phylogeny, and disease associations of the mucin pangenome.},
journal = {medRxiv : the preprint server for health sciences},
volume = {},
number = {},
pages = {},
pmid = {42428052},
abstract = {Mucins are large glycoproteins that provide hydration and barrier function to epithelial tissues. Although genetically heterogeneous, all mucins harbor a large exon composed of variable number tandem repeats (VNTRs). Short-read sequencing has limited our understanding of mucin VNTR diversity and makes disease association studies challenging. We leverage 296 long-read phased genome assemblies to characterize 14 mucin family members, achieving ≥97% accuracy across 572 haplotypes. Phylogenetic haplogroup analysis reveals extraordinary structural heterozygosity, with MUC4 harboring the greatest allelic diversity (n=240 distinct lengths) and MUC12 the greatest size range (Δ = 55,233 bp; 23,080 amino acids). Ten mucins show significant population stratification (pFDR < 0.05). At the MUC4/MUC20 locus, we characterize higher-order structural variation, including a recurrent inversion, copy number variation, and interlocus gene conversion. Optimized genotyping achieves ≥95% haplogroup concordance across 10 loci. We apply this to 4,637 deeply phenotyped cystic fibrosis patients and identify a significant association between short MUC1 VNTRs and severe disease (p=0.0056), demonstrating the pangenome's utility for complex locus genotyping and disease discovery.},
}

@article {pmid42687919,
year = {2026},
author = {Yaseen, F and Hippe, DS and Cui, S and Fu, J and Kim, Y and Grassberger, C and Deng, L and Ye, T and Kinahan, PE and Zeng, J and Gennari, JH and Bowen, SR},
title = {Toward uncertainty-aware clinical decision support for treatment response prediction in metastatic NSCLC: integrating FDG-PET, T-cell repertoire, and cytokines with conformal prediction.},
journal = {Research square},
volume = {},
number = {},
pages = {},
pmid = {42687919},
issn = {2693-5015},
support = {R01 CA258997/CA/NCI NIH HHS/United States ; },
abstract = {BACKGROUND: Variable response to chemoimmunotherapy in metastatic non-small cell lung cancer (mNSCLC), together with the limited discriminative accuracy of PD-L1 tumor proportion score, highlights the need for reliable, uncertainty-aware early response prediction using multimodal biomarkers. We developed and prototyped a multimodal clinical decision support (CDS) framework integrating longitudinal FDG-PET, T-cell receptor (TCR), and cytokine biomarkers with conformal prediction to deliver uncertainty-quantified, patient-level response predictions.

METHODS: Thirty-five patients with mNSCLC receiving first-line carboplatin-pemetrexed-pembrolizumab on the PET-BRIGHT trial (NCT04151940) underwent FDG-PET/CT and blood collection at baseline and week 3. Multimodal biomarkers included FDG-PET metrics (standardized uptake value/total lesion glycolysis), TCR diversity metrics, and inflammatory cytokines. Nested leave-one-out cross-validation with automated feature selection identified a single biomarker per modality. Class-balanced logistic regression was used for classification, with discrimination assessed by the area under the receiver operating characteristic curve (AUROC) and calibration by the Brier score. Conformal prediction (targeting 80% reliability) quantified patient-level uncertainty via prediction sets and singleton rate. Unimodal and multimodal early- and late-fusion models were evaluated using baseline-only and combined baseline plus mid-treatment biomarkers. Models were benchmarked against PD-L1 tumor proportion score, and statistical significance was assessed by permutation testing against an empirical null.

RESULTS: PD-L1 tumor proportion score, the current clinical standard, discriminated poorly (AUROC 0.58, 95% CI 0.39-0.78). At PreTx, unimodal TCR was the strongest single modality (AUROC 0.80), followed by PET (0.76) and cytokines (0.54). Late fusion of PET and TCR achieved the highest PreTx discrimination (0.85) and increased singleton predictions from 78% to 89%. After incorporating mid-treatment biomarkers, cytokines became the strongest single modality (0.78) while TCR was attenuated (0.66); late fusion of PET and cytokines achieved the highest discrimination overall (0.86). Thirteen of 22 model and timepoint combinations exceeded a permutation null at p < 0.05, and empirical coverage was 78% and 82% against an 80% target.

CONCLUSIONS: A multimodal framework combining longitudinal biomarkers with conformal prediction substantially outperformed the current clinical standard while identifying patients for whom a confident prediction could not be made. A prototype CDS interface demonstrates feasibility for clinical translation.

TRIAL REGISTRATION: ClinicalTrials.gov NCT04151940, registered 26 September 2019.},
}

@article {pmid42690663,
year = {2026},
author = {Elia, MV and Friesner, ID and Kwon, D and Ni, L and Sinha, S and Ishiyama, Y and Zack, T and Bridge, M and Fong, L and Hong, JC},
title = {Large Language Models and Adverse Event Detection Within Immunotherapy Clinical Trials.},
journal = {JAMA network open},
volume = {9},
number = {9},
pages = {e2631840},
pmid = {42690663},
issn = {2574-3805},
}

@article {pmid42691161,
year = {2026},
author = {Minervina, AA and Pogorelyy, MV and Mayer-Blackwell, K and Tirtakusuma, R and Schattgen, SA and Fiore-Gartland, A and Walczak, AM and Mora, T and Bradley, P and Thomas, PG},
title = {Uneven TCR chain pairing constraints govern epitope recognition.},
journal = {Science (New York, N.Y.)},
volume = {393},
number = {6815},
pages = {eadx3863},
doi = {10.1126/science.adx3863},
pmid = {42691161},
issn = {1095-9203},
mesh = {Humans ; Amino Acid Sequence ; *Epitopes, T-Lymphocyte/immunology/chemistry ; *Receptors, Antigen, T-Cell, alpha-beta/chemistry/immunology/genetics ; T-Cell Antigen Receptor Specificity ; Jurkat Cells ; K562 Cells ; HEK293 Cells ; },
abstract = {Combinatorial pairing of independently recombined T cell receptor (TCR) α- and β-chains is central to diversifying the TCR repertoire. Although sequence motifs in one chain correlate with epitope recognition, the extent to which a single chain dictates specificity remains unclear. Here, we systematically tested TCR chain coupling constraints by enforcing the pairing of individual chains with hundreds of thousands of partners. Although most chains paired stably, the preservation of epitope specificity was rare and highly variable, with the frequency of compatible partners ranging from ~10 to <0.1%. This approach identified >70,000 epitope-specific TCRs across 10 epitopes. Our work illuminates the distinct contributions of TCR chains, highlights the limitations of single-chain data, and provides an experimental and analytical framework for refining TCR-peptide-major histocompatibility complex specificity inference.},
}

Humans
Amino Acid Sequence
*Epitopes, T-Lymphocyte/immunology/chemistry
*Receptors, Antigen, T-Cell, alpha-beta/chemistry/immunology/genetics
T-Cell Antigen Receptor Specificity
Jurkat Cells
K562 Cells
HEK293 Cells

@article {pmid42692015,
year = {2026},
author = {Hysong, MR and Shuey, MM and Miller-Fleming, TW and Keat, K and Stilp, AM and Li, Y and Cox, NJ and Auer, PL and Franceschini, N and Verma, A and Raffield, LM and Reiner, AP},
title = {Phenome- and laboratory-wide meta-analyses of sickle cell trait reveal multi-system disease associations.},
journal = {American journal of human genetics},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.ajhg.2026.08.010},
pmid = {42692015},
issn = {1537-6605},
support = {R01 HL146500/HL/NHLBI NIH HHS/United States ; U01 HG011720/HG/NHGRI NIH HHS/United States ; },
abstract = {Sickle cell trait (SCT) is increasingly recognized as a risk factor for adverse health outcomes. We utilized three large US electronic health record-based biobanks (Vanderbilt University Medical Center's BioVU, Penn Medicine Biobank, and All of Us) to conduct phenome-wide association (PheWAS) and clinical laboratory-wide association (LabWAS) meta-analyses of 4,813 individuals with SCT among 58,830 African genetic ancestry participants (∼60% female). Significant associations were replicated using a published PheWAS of SCT from the Million Veteran Program. Our PheWAS meta-analysis confirmed the association of SCT with increased risks of kidney disease, pulmonary embolism, and anemia, while also identifying associations with increased risk of splenomegaly, gout, acute pyelonephritis, and anemia of pregnancy. LabWAS confirmed prior associations of SCT with blood cell counts, red cell indices, kidney function, and urinary concentrating ability. We also identified associations with higher serum electrolytes, bilirubin, and reticulocyte count and lower blood urea nitrogen and platelet count. In sex-stratified analyses, the association of SCT with kidney-related disorders and kidney dysfunction was stronger in females, while the association with platelet and lymphocyte phenotypes was greater in males with SCT. Our results provide insights into the multi-system complications of SCT and have potential clinical implications both for general awareness of susceptibility and appropriate reference ranges for various clinical laboratory parameters in individuals with SCT.},
}

@article {pmid42693364,
year = {2026},
author = {Lu, AZ and Yi, JC and Henrikson, NB and Panattoni, LE and Lowry, D and Harkey, K and Jones, SMW},
title = {Examination of insurance type and cancer treatments with administrative burdens and financial toxicity in a sample of cancer survivors.},
journal = {Journal of cancer survivorship : research and practice},
volume = {},
number = {},
pages = {},
pmid = {42693364},
issn = {1932-2267},
abstract = {PURPOSE: Many cancer survivors experience administrative burdens and poor financial outcomes but associations with insurance and cancer treatments are not well studied. This study aimed to fill that gap.

METHODS: Cancer survivors (n = 459), on average 11 years post-diagnosis and in the United States completed a cross-sectional survey. Dependent variables were five types of insurance-related administrative burdens (prior authorization, denials, surprise bills, stepped care, out-of-network care) and four dimensions of financial toxicity. Independent variables were health insurance type at diagnosis and cancer treatments. Logistic and linear regression models assessed the relationships between independent and dependent variables.

RESULTS: Forty-six percent reported at least one insurance-related administrative burden. Participants who received immunotherapy (prior authorizations: 33%; surprise bills: 46%; stepped care: 26%), chemotherapy (denial: 22%; stepped care: 17%), surgery (surprise bills: 33%; out-of-network: 16%) and radiation therapy (denials: 24%) reported significantly higher prevalence of administrative burdens than those who had not received those treatments (p's < 0.05). Insurance type was not associated with administrative burdens (p's > 0.05). Surgery, chemotherapy and immunotherapy were associated with more financial coping than those who did not receive these treatments (p's < 0.025). Compared to employer/school-sponsored insurance, most insurance types were not associated with financial toxicity except self-purchased insurance was associated with more financial depression, anxiety and coping (p's < 0.05).

CONCLUSIONS: Patient-reported administrative burden may be associated with all types of insurance and survivors may respond with more financial coping.

Immunotherapy and chemotherapy may have the highest risk for administrative burdens but surgery and radiation therapies can also confer risk.},
}

@article {pmid42694742,
year = {2026},
author = {Lubwama, M and Gulleen, E and Sekyanzi, S and Asiimwe, B and Njai, A and Winter, J and Hoyles, L and Niyonzima, N and Orem, J and Ddungu, H and Kambugu, J and Nakaganda, A and Kateete, DP and Phipps, W and Bwanga, F},
title = {The urgent need to integrate infectious diseases expertise into the management of cancer patients with infections in sub-Saharan Africa in the era of antimicrobial resistance: a policy brief.},
journal = {Frontiers in pharmacology},
volume = {17},
number = {},
pages = {1889223},
pmid = {42694742},
issn = {1663-9812},
abstract = {Antimicrobial resistance (AMR) is a global health concern. Cancer patients are 1.5-2 times more likely to be affected by AMR than other patient groups. This policy brief, informed by microbiological studies conducted at the Uganda Cancer Institute since 2014, presents key recommendations and implementation strategies for the management of bacterial infections in cancer patients in sub-Saharan Africa (SSA). Our recommendations include strengthening AMR surveillance, implementing context-specific infection prevention and control and antimicrobial stewardship programs, and raising awareness of AMR in cancer in the health sector and community in SSA. A collaborative multidisciplinary approach which includes infectious diseases expertise is required to effectively implement health policies and guidelines. Proactive and effective health policies which address AMR in cancer are critical in cancer centers in SSA.},
}

@article {pmid42697914,
year = {2026},
author = {Choi, C and Labriola, M and Henderson, N and Chu, A and Hwang, C and Barata, PC and Cackowski, FC and Broderick, A and McKay, RR and Bilen, MA and Kilari, D and Graham, LS and Tripathi, A and Garje, R and Koshkin, VS and Dorff, TB and Schweizer, MT and Reichert, ZR and Sokolova, AO and Marshall, CH and Armstrong, AJ},
title = {Association between smoking, tumor genetics, and outcomes in men with metastatic prostate cancer.},
journal = {Prostate cancer and prostatic diseases},
volume = {},
number = {},
pages = {},
pmid = {42697914},
issn = {1476-5608},
support = {NIH/NCI 5R01CA233585 - 05//U.S. Department of Health & Human Services | NIH | National Cancer Institute (NCI)/ ; },
abstract = {PURPOSE: Smoking has been associated with increased metastatic prostate cancer mortality, but the mechanisms behind this are largely unknown. We hypothesized that smoking increases the risk of genetic alterations associated with aggressive disease and/or the transformation to neuroendocrine prostate cancer (NEPC).

PATIENTS AND METHODS: We utilized the Prostate Cancer Precision Medicine Multi-institutional Collaborative Effort (PROMISE) clinical genomic database for this retrospective analysis. We associated patient characteristics and tumor genetic data with smoking exposure at diagnosis (current, former, never and pack years) and with clinical outcomes, including overall survival (OS) from diagnosis or time to developing metastatic disease and NEPC status.

RESULTS: We identified 2353 men with prostate cancer and next generation somatic tumor sequencing evaluable for analysis in PROMISE, including 8% current, 39% former, and 52% never smokers. Current smokers were more likely to be younger and to have metastatic (M1 or N1) disease at diagnosis, and less likely to have prior local therapy (all p < 0.001). Current smoking was associated with worse OS from diagnosis (99.9 mo vs 137.6 mo, HR 1.42, 95% CI 1.14-1.77), which remained significant after adjusting for disease characteristics. We found no difference in the percentage of NEPC at initial diagnosis or at any time between current, former, and never smokers (p = 0.8). We found positive associations between smoking status and genetic alterations in SPOP (current: 15%, former 6.7%, never 3.8%; p = 0.018), FGFR1 (current 10%, former 0.4%, never 1.1% p = 0.001), and ARID1A (current 5.1%, former 2.2%, never 0.4%; p = 0.035) in patients with metastatic androgen pathway modulator sensitive prostate cancer (APMS).

CONCLUSION: Active smoking is associated with worse overall and prostate cancer specific survival as compared to never/former smoking and was associated with specific tumor genetic alterations but not small cell/NEPC transformation.},
}

@article {pmid42699539,
year = {2026},
author = {Liu, VM and Othus, M and Naru, J and Ries, RE and Pogosova-Agadjanyan, EL and Appelbaum, FR and Chauncey, TR and Dietrich, E and Erba, HP and Godwin, JE and Fitzgibbon, MP and Fang, M and Lee, SC and Moseley, A and Percival, ME and Qin, G and Radich, JP and Raychaudhuri, S and Willman, CL and Meshinchi, S and Stirewalt, DL},
title = {Prognostic impact of age and MDS-associated mutations in NPM1-mutated AML.},
journal = {Blood neoplasia},
volume = {3},
number = {4},
pages = {100272},
pmid = {42699539},
issn = {2950-3280},
support = {T32 HL007093/HL/NHLBI NIH HHS/United States ; P30 CA015704/CA/NCI NIH HHS/United States ; R01 CA190661/CA/NCI NIH HHS/United States ; U10 CA180888/CA/NCI NIH HHS/United States ; U10 CA180819/CA/NCI NIH HHS/United States ; R01 CA160872/CA/NCI NIH HHS/United States ; U24 CA196175/CA/NCI NIH HHS/United States ; },
abstract = {Nucleophosmin-1 (NPM1) mutations define a major molecular subtype of acute myeloid leukemia (AML) and is generally associated with favorable prognosis. However, the impact of myelodysplastic syndrome-associated mutations (MDS[m+]) on patient outcomes within this subgroup remains uncertain. We retrospectively analyzed 271 patients with NPM1-mutated AML from 3 independent cohorts (SWOG, Fred Hutch, and Beat AML) to assess the prognostic significance of MDS[m+] and its interaction with age. MDS[m+] occurred in 17% of patients, most commonly involving SRSF2 and SF3B1. Although MDS[m+] was associated with inferior overall survival (OS) compared with MDS[m-] in European LeukemiaNet (ELN) 2022 favorable-risk patients (hazard ratio [HR], 2.0; P = .008), this effect was largely driven by worse outcomes in older patients (≥65 years) as older ELN2022 favorable-risk patients had poor OS regardless of the presence of MDS[m+] compared with younger patients. After stratification of patients by age, there was not a significant difference between MDS[m+] and MDS[m-] in either younger patients (HR, 0.99; P = .98) or older patients (HR, 1.42; P = .33). These findings indicate that MDS[m+] in NPM1 [+] AML is not independently associated with adverse risk after adjusting for age, and highlight the need for age-adjusted AML risk models.},
}

@article {pmid42327193,
year = {2026},
author = {DeJong, CS and Frutoso, M and Potchen, NB and Daggupati, G and Konecny, AJ and Huang, Y and Setty, M and Shree, S and McCartney, SA and Prlic, M},
title = {Human tissue-resident CD8 T cells contribute to trophoblast homeostasis in health and during acute inflammation.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
pmid = {42327193},
issn = {2692-8205},
abstract = {Previous studies have highlighted that some T cell subsets in tissues can provide signals to support tissue cell homeostasis and differentiation. If and how T cell-tissue cell signaling is altered in healthy compared to inflamed tissues is poorly understood. Here, we address if communication between human T cells and tissue cells changes from steady state to an acutely inflamed state in the human placenta. We used single cell analysis strategies to examine invasive cytotrophoblasts (iCTBs) and immune cells isolated from third trimester healthy and acutely inflamed human placentas. We performed cell communication analysis to predict cell-cell communication networks, and found evidence that iCTBs provided signals to support the recruitment of T cells, as well as the formation of tissue-resident memory CD8 T cells (Trm). In exchange, Trm provide signals to support iCTB homeostasis. During acute inflammation, iCTBs and macrophages underwent profound transcriptional changes, while most T cell subsets only underwent limited transcriptional changes. This was not due to T cell exhaustion or tolerance, as T cells were functionally intact. Cell communication analysis and validation at the protein level provide evidence that T cells can maintain their homeostatic support to iCTBs during acute inflammation.},
}

@article {pmid42428077,
year = {2026},
author = {Ortblad, KF and Meisner, A and Omollo, V and Kareithi, T and Roche, SD and Ong'wen, P and Asewe, M and Anyona, MO and Banerjee, P and Curran, K and Gichuru, E and Harkey, K and Juma, L and Kiptinness, C and Malen, RC and Mugambi, ML and Otieno, P and Pintye, J and Rono, B and Schaafsma, TT and Shah, PD and Sharma, M and Thomas, KK and Yu, K and Were, D and Bukusi, EA and Ngure, K},
title = {Effectiveness of pharmacy-based HIV pre- and post-exposure prophylaxis delivery: a cluster-randomized trial in Kenya.},
journal = {medRxiv : the preprint server for health sciences},
volume = {},
number = {},
pages = {},
pmid = {42428077},
abstract = {Private pharmacies are ubiquitous yet underutilized for HIV pre- and post-exposure prophylaxis (PrEP and PEP) delivery. In a cluster-randomized trial in Kenya (NCT05842122), we randomized 60 pharmacies 1:1:1:1 to: client-sustained delivery (~$2/visit user fee); implementor-sustained delivery (~$2/visit reimbursement); counselor-supported delivery (task shifting; ~$1/visit reimbursement); or clinic referral (control; ~$1/referral reimbursement). Commodities were supplied free to pharmacies from government stock. Primary outcomes were PrEP initiation and one-month continuation (any dispensing or refilling, respectively), self-reported by clients 60 days post-enrollment (multiple-comparisons threshold: p=0.017). From June 2023-April 2025, 5,808 clients enrolled; 64% were PEP candidates. Compared to referral, the counselor-supported arm had significantly higher PrEP initiation (RR=6.5, 95% CI [2.6, 16], p<0.001) and continuation rates (RR=5.1, 95% CI [1.4, 19], p=0.016); all intervention arms had significantly higher PEP initiation rates. One seroconversion, one social harm, and two provider needlestick injuries occurred. Pharmacy PrEP/PEP delivery outperformed clinic referral, particularly when fully subsidized and counselor-supported.},
}

@article {pmid42679899,
year = {2026},
author = {Prentice, RL and Aragaki, AK and Lampe, JW and Neuhouser, ML and Manson, JE and Raftery, D and Nagana Gowda, GA and Huang, Y and Tinker, LF and Navarro, SL and Lane, DS and Zheng, C},
title = {Serum-based biomarker development for dietary macronutrient densities and their association with breast and colorectal cancer risk in a cohort of postmenopausal females.},
journal = {The American journal of clinical nutrition},
volume = {},
number = {},
pages = {101506},
doi = {10.1016/j.ajcnut.2026.101506},
pmid = {42679899},
issn = {1938-3207},
abstract = {BACKGROUND: Associations of the macronutrient composition of the diet with risks of postmenopausal breast and colorectal cancer (CRC) are uncertain, partly because of reliance on self-reported dietary data.

OBJECTIVES: We aimed to study biomarker development for several macronutrient component densities using serum and spot urine metabolomics and, when appropriate, to assess their associations with breast cancer and CRC risks in a Women's Health Initiative (WHI) cohort of postmenopausal U.S. females.

DESIGN AND METHODS: We explored linear biomarker equations for log-transformed macronutrient component densities using fasting serum metabolomic profiles, with and without spot urine, in a WHI feeding study (n=153). We used equations satisfying a cross-validated regression R[2] (CV-R[2]) criterion to calculate potential biomarker values for 577 breast cancer cases and 181 colorectal cancer cases and their 1-1 matched controls. We used Cox regression with baseline stratification on matched pairs to examine dietary composition associations with cancer risk.

RESULTS: Serum-based biomarker equations for macronutrient component densities had CV-R[2] values as follows: polyunsaturated fatty acids (PUFA) 46.7%, monounsaturated fatty acids (MUFA) 36.3%, saturated fatty acids (SFA) 33.6%, carbohydrate 32.3%, and protein 29.4%. The inclusion of spot urine metabolites did not materially improve these values. In analyses including serum-based PUFA, MUFA, SFA and carbohydrate densities the breast cancer hazard ratios (95% CIs) for 20% increments in dietary densities were 0.98 (0.89, 1.07) for PUFA and 1.14 (0.97, 1.33) for MUFA. Corresponding CRC hazard ratios were 0.98 (0.81, 1.17) and 1.46 (1.10, 1.93). Analyses based on food frequency questionnaires differed from these estimates for breast cancer, but tended to agree for CRC. Intakes of dairy and meat products may help to explain observed associations.

CONCLUSIONS: In a population of U.S. postmenopausal females dietary MUFA density was associated with an elevation in CRC risk. Breast cancer associations with biomarker-based macronutrient densities require further development This study is registered with clinicaltrials.gov identifier: NCT00000611 https://clinicaltrials.gov/study/NCT00000611.},
}

@article {pmid42681418,
year = {2026},
author = {Bailey, SL and Bochenek, M and Youngs, D and Gimferrer, I and Stolla, M},
title = {Tracking and Testing Transfused Versus Endogenous Platelets with Biotin or Human Leukocyte Antigen.},
journal = {Methods in molecular biology (Clifton, N.J.)},
volume = {3053},
number = {},
pages = {243-260},
pmid = {42681418},
issn = {1940-6029},
mesh = {Humans ; *Blood Platelets/metabolism/immunology/cytology ; *Platelet Transfusion/methods ; *HLA Antigens/metabolism/immunology ; Flow Cytometry/methods ; *Biotin/metabolism ; Biotinylation/methods ; },
abstract = {Platelet transfusions are a critical and life-saving intervention utilized in bleeding patients and those at risk of bleeding. The laboratory assessment of fresh or stored platelets, both before and after transfusion, is of interest in licensing and basic science research. Platelets can be given either allogeneic (i.e., from a genetically different donor) or autologous (i.e., donor and recipient are the same, or genetically identical). In this protocol, we demonstrate how to distinguish circulating endogenous platelets from transfused platelets using biotinylation (useful for autologous and allogeneic transfusions) and HLA antibodies (practical in allogeneic transfusion scenarios) to differentiate between circulating endogenous and transfused platelets. Our described methodology not only enables the tracking of platelets but also facilitates post-transfusion functional assessment and the evaluation of platelet function post-transfusion using flow cytometry.},
}

Humans
*Blood Platelets/metabolism/immunology/cytology
*Platelet Transfusion/methods
*HLA Antigens/metabolism/immunology
Flow Cytometry/methods
*Biotin/metabolism
Biotinylation/methods

@article {pmid42681967,
year = {2026},
author = {Smolen, KK and De Paris, K and Angelidou, A and Martin, TM and van Haren, SD and Levy, O},
title = {Development of adjuvanted HIV vaccines tailored for early life: immunologic rationale, clinical experience, and future directions.},
journal = {Current opinion in HIV and AIDS},
volume = {},
number = {},
pages = {},
doi = {10.1097/COH.0000000000001068},
pmid = {42681967},
issn = {1746-6318},
abstract = {PURPOSE OF REVIEW: This review highlights the rationale for and clinical experience in advancing age-specific adjuvantation systems to develop well tolerated and effective pediatric HIV vaccines.

RECENT FINDINGS: Due to both cellular and soluble factors, infant immunity is distinct from that of older children and adults, featuring Th2 bias, tolerogenic APC programming, and reduced Tfh support. Due to distinct functional responses downstream of pattern recognition receptor signaling, adjuvant action is age-specific. Despite a growing pipeline of adjuvants and increasing interest in developing early-life immunization strategies against HIV, few adjuvants have been rigorously evaluated for use in pediatric HIV vaccines. In line with FDA Modernization Act 2.0, systems vaccinology and age-specific immunoprofiling in vivo and in vitro can inform down selection and optimization of age-specific adjuvanted HIV vaccine formulations. Several adjuvants have been assessed as components of HIV vaccines in infants including Alum, the oil-in-water emulsion MF59 and the TLR4 agonist glucopyranosyl lipid A (GLA).

SUMMARY: There is strong rationale to develop an infant HIV vaccine to provide early-life protection, and several adjuvants have been assessed thus far in early-phase clinical studies. With a growing adjuvant pipeline, much work remains to assess which adjuvants should be advanced for an infant HIV vaccine. Leveraging age-specific preclinical studies including immune profiling and human in-vitro modeling can inform down selection to identify adjuvantation systems offering safety and antigen dose sparing, while enhancing breadth and durability of vaccine immunogenicity.},
}