@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.},
}

@article {pmid42685296,
year = {2026},
author = {Kronenberg, Z and Yoo, B and Chua, KP and Chaisson, MJP and Lansdon, L and Rowell, WJ and Brandine, GS and Bruand, J and Dolzhenko, E and Ikegami, K and Sarthy, J and Huang, KK and Tan, P and Bhise, S and Fan, E and Mendoza, M and O'Donnell, E and Pastinen, T and Lawlor, ER and Furlan, SN and Farooqi, MS and Eberle, MA},
title = {Hunting for microsatellite instability in long-read data with Owl.},
journal = {PLoS computational biology},
volume = {22},
number = {9},
pages = {e1014423},
doi = {10.1371/journal.pcbi.1014423},
pmid = {42685296},
issn = {1553-7358},
abstract = {Microsatellite instability (MSI) is a key biomarker of mismatch repair deficiency and response to immunotherapy, yet most existing genomic detection methods are optimized for short-read sequencing and rely on a panel of homopolymer markers, limiting the ability to characterize genome-wide and motif-specific patterns of instability. Here we present Owl, a bioinformatic tool for quantifying MSI from long-read (PacBio) genomic data. Owl leverages a genome-wide marker set of more than 140,000 microsatellite repeats ranging from 1-6 bp in length to measure MSI across a phased genome. Using a wrap-around alignment algorithm, Owl constructs repeat-length distributions at each marker site and flags somatic instability using the coefficient of variation. We applied Owl to screen for markers with stable coverage, phasing, and baseline variation across 131 diverse genomes from the Human Pangenome Reference Consortium, where Owl scores ranged from 1.4% to 5.4% of markers exceeding the instability threshold. When applied to cancer cell lines and one diffuse astrocytoma tumor-normal pair, Owl identified six MSI genomes with 10-27% unstable markers and showed close concordance with an Illumina DRAGEN MSI assay for the astrocytoma sample. Motif-level analyses revealed shared enrichment of short homopolymer and dinucleotide (A- and AT-rich) repeats across MSI cancers. Owl is implemented in Rust and integrated into the PacBio HiFi Somatic workflow, providing a scalable framework for MSI analysis from long-read sequencing focused on repeat instability specifically in tumor samples.},
}

@article {pmid42686173,
year = {2026},
author = {Bricker, JB and Santiago-Torres, M and Sullivan, BM and Mull, KE and Clark, HW and Kornacki, C and Afraid Of Lightning-Craddock, T and Seneca, DS and Stanford, CM and Wilcox, SL and Henderson, PN and Nelson, L},
title = {A Culturally Adapted Smoking Cessation App (IndigeQuit) for American Indian and Alaska Native Adults: Protocol for a Randomized Clinical Trial.},
journal = {JMIR research protocols},
volume = {15},
number = {},
pages = {e102675},
doi = {10.2196/102675},
pmid = {42686173},
issn = {1929-0748},
mesh = {Adult ; Female ; Humans ; Alaska Natives/psychology/statistics & numerical data ; *American Indian or Alaska Native/psychology/statistics & numerical data ; Community-Based Participatory Research ; *Mobile Applications/standards ; Randomized Controlled Trials as Topic ; *Smoking Cessation/methods/ethnology ; Male ; },
abstract = {BACKGROUND: Due to limited access to evidence-based cessation support, American Indian and Alaska Native (AI/AN) adults are half as likely to quit commercial cigarette smoking as other racial and ethnic groups. Geographical barriers, underfunded health systems, and limited integration of cessation services into routine care have reduced access to effective treatment in AI/AN communities. These challenges are compounded by a lack of culturally relevant interventions tailored to AI/AN adults. Thus, there is an urgent need for accessible, scalable, and culturally relevant interventions.

OBJECTIVE: Here, we describe the protocol for a randomized clinical trial (RCT) testing the efficacy of a culturally adapted smoking cessation app (IndigeQuit) developed specifically to help AI/AN adults quit smoking commercial cigarettes compared to a standard, nontailored app (QuitGuide).

METHODS: To improve the relevance and acceptability of cessation support to AI/AN adults, IndigeQuit was developed through a cultural adaptation of iCanQuit, an evidence-based smartphone app grounded in acceptance and commitment therapy that teaches skills for accepting cravings to smoke. The cultural adaptation used a user-centered, community-based participatory research mixed methods approach in collaboration with a community advisory board (CAB) comprising AI/AN individuals. Cultural adaptations included the use of Native imagery; stories featuring AI/AN adults and elders emphasizing culture, spirituality, family, and community; and the important distinction between ceremonial and commercial tobacco. A total of 776 AI/AN adults who smoke and want to quit are being recruited nationwide and randomized to receive IndigeQuit or QuitGuide for 12 months. The primary aim of the RCT is to determine the efficacy of IndigeQuit compared with QuitGuide for 30-day abstinence at 12 months. Secondary aims include abstinence at earlier time points, identifying mediators and moderators of treatment effects, and assessing engagement and satisfaction. Qualitative interviews with IndigeQuit participants and CAB members will inform the development of a subsequent guide to support the broad dissemination of IndigeQuit nationwide.

RESULTS: The National Cancer Institute funded this study in 2024 (grant R01 CA284687), with the grant awarded to the principal investigator, JBB. As of August 2026, a total of 590 AI/AN adults had been enrolled in the trial. Data collection started in July 2025 and is expected to be completed by November 2028.

CONCLUSIONS: The IndigeQuit app was designed to deliver evidence-based smoking cessation treatment that is culturally adapted to AI/AN communities and grounded in acceptance and commitment therapy. If effective, this intervention could offer a more scalable and culturally relevant treatment to AI/AN communities nationwide, helping to reduce smoking-related health inequities.

TRIAL REGISTRATION: ClinicalTrials.gov NCT06145763; https://clinicaltrials.gov/study/NCT06145763.

DERR1-10.2196/102675.},
}

Adult
Female
Humans
Alaska Natives/psychology/statistics & numerical data
*American Indian or Alaska Native/psychology/statistics & numerical data
Community-Based Participatory Research
*Mobile Applications/standards
Randomized Controlled Trials as Topic
*Smoking Cessation/methods/ethnology
Male

@article {pmid42686770,
year = {2026},
author = {Jiang, M and Hu, C and Hedouin, S and Andrade Latino, A and Arimura, Y and Stergachis, AB and Biggins, S},
title = {Native yeast kinetochore structures identify an essential inner kinetochore interaction.},
journal = {Nature communications},
volume = {17},
number = {1},
pages = {},
pmid = {42686770},
issn = {2041-1723},
support = {R35 GM149357/GM/NIGMS NIH HHS/United States ; R35 GM149357//U.S. Department of Health & Human Services | National Institutes of Health (NIH)/ ; },
mesh = {*Kinetochores/metabolism/ultrastructure ; *Saccharomyces cerevisiae/metabolism/genetics ; *Saccharomyces cerevisiae Proteins/metabolism/genetics/chemistry ; Cryoelectron Microscopy ; Centromere/metabolism ; Nucleosomes/metabolism ; Chromosome Segregation ; DNA, Fungal/metabolism ; Nuclear Proteins/metabolism/genetics ; },
abstract = {Kinetochores must accurately assemble on centromeres for faithful chromosome segregation. Although a conserved centromeric nucleosome is essential for kinetochore assembly, budding yeast centromeric DNA is a poor template for nucleosome formation in vitro, perhaps due to its intrinsic rigidity. To better understand yeast inner kinetochore assembly, we develop a one-step protocol to purify native inner kinetochore subcomplexes for structural studies. We perform cryoelectron microscopy on the purifications and generate density maps of four separate inner kinetochore complexes, two of which have not been previously visualized and may represent intermediate assemblage states. We identify an Ndc10 trimerization domain that engages centromeric DNA and a pair of CBF3 complexes and is associated with substantial bending of centromeric DNA. Ndc10 trimerization is essential for kinetochore assembly and chromosome segregation. We propose that Ndc10 trimerization facilitates centromeric DNA bending to stabilize the centromeric nucleosome and inner kinetochore.},
}

*Kinetochores/metabolism/ultrastructure
*Saccharomyces cerevisiae/metabolism/genetics
*Saccharomyces cerevisiae Proteins/metabolism/genetics/chemistry
Cryoelectron Microscopy
Centromere/metabolism
Nucleosomes/metabolism
Chromosome Segregation
DNA, Fungal/metabolism
Nuclear Proteins/metabolism/genetics

@article {pmid42687809,
year = {2026},
author = {Zarnegar-Lumley, S and Pommert, L and Lacayo, NJ and Petit, A and Shukla, N and Stevens, A and Gibson, A and Tarlock, K},
title = {Real-world experience with IDH inhibitors in pediatric patients with IDH1- and IDH2-mutated acute myeloid leukemia and myelodysplastic syndrome.},
journal = {Haematologica},
volume = {},
number = {},
pages = {},
doi = {10.3324/haematol.2026.301245},
pmid = {42687809},
issn = {1592-8721},
abstract = {Not available.},
}

@article {pmid42676126,
year = {2026},
author = {Lange, J and Etzioni, R},
title = {Mining Stored-Specimen Studies for Information about Cancer Natural History.},
journal = {Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology},
volume = {35},
number = {9},
pages = {1484-1486},
doi = {10.1158/1055-9965.EPI-26-0731},
pmid = {42676126},
issn = {1538-7755},
mesh = {Humans ; *Neoplasms/diagnosis/blood ; *Early Detection of Cancer/methods ; Bayes Theorem ; *Data Mining/methods ; },
abstract = {The advent of new multicancer early detection tests and publication of early diagnostic results have generated expectations of clinical benefit from multicancer screening. The clinical benefit of a cancer screening test depends critically on disease natural history, which is typically learned from prospective screening studies. Retrospective studies of stored blood specimens are important in learning about a test's preclinical diagnostic performance but have rarely been used to infer natural history. The extent to which these studies might be harnessed to also learn natural history is discussed in the context of an article in this issue that infers the combined natural history of a range of cancers targeted by a multicancer early detection test using a case-control subsample of specimens from a large cohort study. The critical question concerns the identifiability of key transition rates in multistate models of natural history alongside state-specific sensitivities. The article suggests that these parameters are estimable within a Bayesian framework that leverages prior information about test sensitivity from diagnostic studies. We offer a heuristic discussion of identifiability in this setting and encourage formal study to determine the extent to which models with varying degrees of complexity may be learned from stored-specimen studies. See related article by Dai et al., p. 1535.},
}

Humans
*Neoplasms/diagnosis/blood
*Early Detection of Cancer/methods
Bayes Theorem
*Data Mining/methods

@article {pmid42678155,
year = {2026},
author = {Chhan, CB and Wan, Y-H and Wilcox-King, A and Homad, LJ and Aldridge, NT and Iureniev, R and Stamatatos, L and McGuire, AT},
title = {Evaluating an anti-idiotype derived germline-targeting immunogen designed to elicit VRC01-class precursors in human antibody transgenic mice.},
journal = {mSphere},
volume = {},
number = {},
pages = {e0031726},
doi = {10.1128/msphere.00317-26},
pmid = {42678155},
issn = {2379-5042},
abstract = {An effective HIV-1 vaccine will likely need to elicit broadly neutralizing antibodies (bNAbs) that bind relatively conserved regions of the otherwise highly variable envelope glycoprotein. Among these, VRC01-class bNAbs are a reproducible antibody class that bind the CD4-binding site through genetic features encoded by the VH1-2 heavy chain and a light chain containing a rare five-amino-acid-long complementarity-determining region 3 (CDRL3). We previously developed a germline-targeting immunogen, iv4/iv9, derived from anti-idiotypic monoclonal antibodies (ai-mAbs) that target these genetic signatures of VRC01-class bNAbs. Here, we applied structure-guided modification of iv4/iv9 that improved selective binding to VRC01 precursors in vitro and carried out immunizations in ATX-GK mice. These mice are transgenic for human antibody genes, producing a diverse, genetically human antibody repertoire. We found that ATX-GK mice harbor VRC01 precursors at frequencies lower than those found in humans. Class-switched VRC01 precursors were detected in a minority of mice immunized with a modified iv4/iv9 immunogen. Collectively, these results indicate that the ATX-GK mice have utility to evaluate VRC01-class germline-targeting immunogens but are a stringent model due to a low frequency of VRC01-class B cells. They further suggest that the ai-mAb immunogens evaluated herein will require further optimization to reproducibly prime VRC01-class B cells in ATX-GK mice.IMPORTANCEAn effective HIV-1 vaccine will likely need to elicit broadly neutralizing antibodies (bNAbs) that bind relatively conserved regions of the otherwise highly variable envelope glycoprotein. Among these, VRC01-class bNAbs are a reproducible antibody class that bind the CD4-binding site through genetic features encoded by the VH1-2 heavy chain and a light chain containing a rare five-amino-acid-long complementarity-determining region 3 (CDRL3). We previously developed a germline-targeting immunogen, iv4/iv9, derived from anti-idiotypic monoclonal antibodies that target these genetic signatures of VRC01-class bNAbs. Here, we evaluate the B-cell response to immunization with iv4/iv9 and with a structure-guided modified iv4/iv9 in ATX-GK mice. These modifications are intended to improve the selectivity of VRC01 precursors in a diverse polyclonal B cell repertoire. These mice are transgenic for human antibody genes, producing a diverse, genetically human antibody repertoire. We found that ATX-GK mice harbor VRC01 precursors at frequencies lower than those found in humans. Class-switched VRC01 precursors were detected in a minority of animals immunized with the modified iv4/iv9. Collectively, these results indicate that although the iv4/iv9 immunogen did not reproducibly elicit VRC01-class B cells, ATX-GK mice have utility to evaluate VRC01-class germline-targeting immunogens but are a stringent model due to a low frequency of VRC01-class B cells.},
}

@article {pmid42678915,
year = {2026},
author = {Birnley, S and Sugrue, MW and Vivero, A and Sica, RA and Kalouche, E and Kota, D and Salzman, D and Smilee, R and Ahmed, I and Modi, A and Klamer, G and Johnson, P and Lynch, J and Warkentin, P and Otegbeye, F},
title = {Sustaining Cell Therapy Quality through Shared Responsibility: A Call for Equitable FACT Inspectorate Participation.},
journal = {Blood advances},
volume = {},
number = {},
pages = {},
doi = {10.1182/bloodadvances.2026019676},
pmid = {42678915},
issn = {2473-9537},
abstract = {This paper highlights a critical challenge in the FACT peer-accreditation system: a growing imbalance between the rising number of accredited and applicant organizations and the limited pool of volunteer inspectors. This imbalance places a disproportionate burden on current inspectors, concentrates accreditation expertise within a small subset of programs, and threatens the efficiency of the peer-review model. The paper presents compelling evidence that organizations contributing to the inspectorate gain measurable benefits. These include stronger audit performance in renewal cycles, access to education in quality standards and best practices, and broader professional networks. The paper concludes with a call to action: accredited organizations should share responsibility and contribute equitably to the FACT inspectorate to maintain the quality and sustainability of the accreditation process.},
}

@article {pmid42667217,
year = {2026},
author = {Muriuki, F and Roach, K and Suh, YJ and Pandey, M and Cheung, BCH and Segall, JE and Wu, M},
title = {A Microfluidic Platform for Studying Roles of Mechanical Compression in Tumor-Immune Cell Interactions in a 3D Extracellular Matrix.},
journal = {Journal of visualized experiments : JoVE},
volume = {},
number = {234},
pages = {},
doi = {10.3791/72929},
pmid = {42667217},
issn = {1940-087X},
mesh = {*Extracellular Matrix/immunology/pathology ; Humans ; *Microfluidic Analytical Techniques/methods/instrumentation ; Spheroids, Cellular/immunology/pathology ; *Killer Cells, Natural/immunology ; Female ; *Breast Neoplasms/immunology/pathology ; MCF-7 Cells ; Cell Communication/immunology ; },
abstract = {Mechanical forces significantly influence the ability of immune cells to kill tumor cells in the context of cell-based immunotherapy. To kill tumor cells, immune cells must exert forces on the target cell and form an immune synapse, through which cytotoxic molecules -including granzyme B-are delivered. Despite their importance, how mechanical cues can be leveraged to enhance immune-mediated killing remains poorly understood. This knowledge gap is partly due to the lack of tools capable of providing well-controlled mechanical stress to cell cultures in a physiologically realistic environment. Here, we describe a microfluidic compression device that can apply static or dynamic compression to tumor spheroids embedded in extracellular matrix (ECM) while enabling real-time imaging of tumor-immune interactions via optical microscopy. The microfluidic platform consists of 12 compartments (6 control and 6 functional). Each compartment contains a cell chamber positioned directly beneath the pressure control unit. Spheroids embedded in ECM are placed within the cell chamber. Using this platform, we investigated the killing efficiency of Natural Killer (NK) cells against breast tumor spheroids (MCF-7) under defined mechanical compression. The results showed that NK cells remained the primary drivers of tumor spheriods death regrardless of mechanical compression in 1.5 mg/mL collagen. Therefore, suggesting that NK cells can maintain their anti-tumor activity under compressive stress. These findings demonstrate the utility of this platform for investigating the role of mechanical forces in tumor-immune interactions. Ongoing studies are identifying the molecular mechanisms that allow immune cells to adapt to compressive stress. Insights gained from these studies may reveal a promising therapeutic avenue.},
}

*Extracellular Matrix/immunology/pathology
Humans
*Microfluidic Analytical Techniques/methods/instrumentation
Spheroids, Cellular/immunology/pathology
*Killer Cells, Natural/immunology
Female
*Breast Neoplasms/immunology/pathology
MCF-7 Cells
Cell Communication/immunology

@article {pmid42667569,
year = {2026},
author = {Abramson, JS and Straus, DJ and Bartlett, NL and Burke, JM and Lynch, RC and Domenech, ED and Hess, B and Schuster, SR and Linhares, Y and Gandhi, M and Shah, HR and Jurczak, W and Re, A and Hahn, U and Prince, HM and Guo, W and Davis, G and Ho, L and Fanale, M and Yasenchak, CA and Lee, HJ},
title = {Summary of Research: Brentuximab Vedotin and Nivolumab in Combination with Chemotherapy for Nonbulky, Early-Stage Classical Hodgkin Lymphoma.},
journal = {Advances in therapy},
volume = {},
number = {},
pages = {},
pmid = {42667569},
issn = {1865-8652},
abstract = {This is a summary of the original research article "Brentuximab Vedotin and Nivolumab in Combination with Chemotherapy for Nonbulky, Early-Stage Classical Hodgkin Lymphoma." The phase 2 SGN35-027 study (NCT03646123) is a multiple-part clinical trial of brentuximab vedotin (BV), with nivolumab, doxorubicin, and dacarbazine (AN + AD), in classical Hodgkin lymphoma (cHL). Here, we present the efficacy and safety of AN + AD from part C of this study in patients with nonbulky, early-stage cHL. At the time of this analysis, 154 patients had received ≥ 1 dose of AN + AD and 98% had received all 4 cycles of treatment. The objective response rate at end of treatment was 96%, and complete response rate was 92% (95% for the favorable subgroup; 91% for the unfavorable subgroup). The proportion of patients with complete response lasting ≥ 2 years was 96%. At a median follow-up of 27.9 months, the estimated 2-year progression-free survival rate was 97%. Any-grade and grade ≥ 3 treatment-related side effects occurred in 97% and 34% of patients, respectively. No events of febrile neutropenia were reported. Any-grade treatment-emergent immune-mediated adverse events occurred in 22% of patients. Collectively, results from this study support the use of BV and nivolumab in combination with limited chemotherapy in patients with nonbulky, early-stage cHL.},
}

@article {pmid42670950,
year = {2026},
author = {Bern-Klug, M and Levine, M and Pope, T and Loggers, E and Wechkin, H},
title = {Minimal Comfort Feeding in Advanced Dementia in the U.S.: Social Work Perspectives and Practice Implications.},
journal = {Journal of social work in end-of-life & palliative care},
volume = {},
number = {},
pages = {1-15},
doi = {10.1080/15524256.2026.2724835},
pmid = {42670950},
issn = {1552-4264},
abstract = {Some people diagnosed with dementia don't want to live through dementia's advanced stages. This article presents a new practice, Minimal Comfort Feeding, and contrasts it with Medical Aid in Dying (MAID), Voluntarily Stopping Eating and Drinking (VSED), VSED-AD (by advance directive), and Comfort Feeding Only (CFO). Also presented are results from a survey of primarily palliative social workers about their opinions regarding MCF. These social workers report potential benefits and challenges with MCF. Practice implications include the need for organizational protocols, staff education and training, as well as appropriate support for all caregivers involved.},
}

@article {pmid42671149,
year = {2026},
author = {Broglio, KR and Krakow, EF and Moodie, EEM},
title = {How to be SMART in oncology: A practical framework to assess the contribution of phase using sequential multiple adaptive randomized treatment designs.},
journal = {Clinical trials (London, England)},
volume = {},
number = {},
pages = {17407745261471462},
doi = {10.1177/17407745261471462},
pmid = {42671149},
issn = {1740-7753},
abstract = {BACKGROUND: Sequential multiple adaptive randomized treatment designs can generate registrational-quality evidence for the contribution of phase in perioperative oncology by preserving randomized comparisons and intent-to-treat estimation while improving efficiency relative to traditional three-arm trials, and yet they remain underappreciated. We present a sequential multiple adaptive randomized treatment design framework for perioperative regimens with neoadjuvant and adjuvant phases, motivated by perioperative immunotherapy in resectable non-small-cell lung cancer, where the benefit of neoadjuvant therapy is hypothesized to be greater than that of adjuvant therapy.

METHODS: We define analyses for perioperative-versus-control, neoadjuvant-only-versus-control, and contribution of phase (incremental adjuvant benefit). We specify intent-to-treat analysis sets and describe unbiased estimation.

RESULTS: In a hypothetical trial calibrated to a perioperative setting, a sequential multiple adaptive randomized treatment design increases the number of events for regimen-versus-control comparisons and isolates a randomized comparison for the contribution of phase at the second randomization. Compared with a traditional multi-arm design, simulations demonstrate controlled family-wise type I error (<0.05) and higher power.

CONCLUSIONS: Sequential multiple adaptive randomized treatment designs provide a principled, practical approach to within-trial contribution of phase in confirmatory oncology. Sequential multiple adaptive randomized treatment designs offer an efficient approach that addresses regulatory concerns and provides valid and robust inference. Because sequential multiple adaptive randomized treatment designs formalize the iterative nature of clinical decision-making, they are uniquely poised to explicitly answer questions related to overtreatment or undertreatment.},
}

@article {pmid42671192,
year = {2026},
author = {Cui, N and Goya, S and Piliper, EA and Greninger, AL},
title = {Integration of an anellovirus genome in the SKNO-1 acute myeloid leukemia cell line.},
journal = {Microbiology spectrum},
volume = {},
number = {},
pages = {e0090426},
doi = {10.1128/spectrum.00904-26},
pmid = {42671192},
issn = {2165-0497},
abstract = {Anelloviruses are highly diverse, ubiquitous single-stranded DNA viruses whose replication, cellular reservoirs, and mechanisms of persistence remain poorly understood. Here, we identify and characterize an Alphatorquevirus homin29 genome stably integrated into an rDNA locus of human chromosome 21 in the acute myeloid leukemia cell line SKNO-1. Large-scale mining of NCBI Sequence Read Archive data sets revealed unusually high anellovirus k-mer abundance specifically in sequencing runs of the SKNO-1 cell line from multiple laboratories. De novo assembly of RNA-Seq data recovered a 3.25 kb viral genome, and long-read PacBio sequencing confirmed its integration within the RNA45SN2 gene on human chromosome 21. Digital droplet PCR (ddPCR) quantified ~0.5 viral genomes per cell, and RT-ddPCR detected transcripts from ORF1 and viral integration-associated flanking repeats, consistent with transcription of the integrant. The ORF1 coding sequence encoded a truncated but structurally conserved capsid protein retaining jelly roll and P-domain features, but lacking the C-terminal domain. Analysis of public ChIP-Seq data from the SKNO-1 cell line demonstrated broad occupancy of the BRD4 transcriptional coactivator across the viral genome, along with focal enrichment of hematopoietic ETS family transcription factors within the integrant's ~300 bp untranslated region upstream of viral open reading frames. Together, these findings demonstrate stable integration, chromatin accommodation, and transcriptional maintenance of an Alphatorquevirus in a human leukemia cell line, providing a unique model to study host tolerance and transcriptional regulation of anellovirus DNA, and informing our understanding of anellovirus hematopoietic cell tropism.IMPORTANCEAnelloviruses are a curious group of single-stranded DNA viruses with substantial genetic diversity that have been found ubiquitously among humans and are hypothesized to be a potential commensal human virus. Their omnipresence has been matched only by the dearth of our understanding of their basic biological processes-how they persist, how they replicate, and how they spread. Here, we identify a naturally integrated Alphatorquevirus genome in the widely used AML cell line SKNO-1 and show that it is stably maintained, transcribed, and embedded within a rDNA locus on human chromosome 21. This discovery highlights the ability of anelloviruses to integrate into human DNA, generates hypotheses around transcription factors used in anellovirus gene transcription, and suggests anelloviruses can persist in myeloblasts.},
}

@article {pmid42673546,
year = {2026},
author = {Zhuo, K and Banerjee, R},
title = {Telehealth and Electronic Messages in Hematology: The Good, the Bad, and the Ugly.},
journal = {JCO oncology practice},
volume = {},
number = {},
pages = {OP2600898},
doi = {10.1200/OP-26-00898},
pmid = {42673546},
issn = {2688-1535},
}

@article {pmid42673762,
year = {2026},
author = {Juraska, M and Li, L and Magaret, CA and Peng, J and Giorgi, EE and Ludwig, J and Carpp, LN and deCamp, AC and Kee, JJ and Molitor, C and Mandig, M and Edlefsen, PT and Rossenkhan, R and Westfall, DH and Deng, W and Chen, L and Zhao, H and Galvao, B and Adams, C and Yssel, A and Matten, D and York, T and Gwashu-Nyangiwe, A and Ndabambi, N and Thebus, R and Swann, EM and Hural, JA and van Duijn, J and Buchbinder, S and Tomaka, F and Corey, L and Mngadi, K and Gray, GE and Gilbert, PB and Williamson, C and Mullins, JI},
title = {Quantifying how HIV-1 envelope sequence features impact vaccine efficacy in the HVTN 705/HPX2008 randomised trial in southern African women.},
journal = {EBioMedicine},
volume = {131},
number = {},
pages = {106459},
doi = {10.1016/j.ebiom.2026.106459},
pmid = {42673762},
issn = {2352-3964},
abstract = {BACKGROUND: A heterologous Ad26.Mos4.HIV and clade C gp140 vaccine regimen did not show overall significant efficacy against HIV-1 acquisition [point estimate 14.1%; 95% confidence interval (CI), -22.0 to 39.5] in the HVTN 705/HPX2008 trial in southern African women. We examined whether and how vaccine efficacy (VE) against HIV-1 diagnosis over 7-24 months post-first dose varied by HIV-1 Envelope (Env) amino acid sequence features.

METHODS: HIV-1 viral sequences were generated by PacBio SMRT-UMI sequencing from the first RNA-positive sample of participants who acquired HIV-1. Env amino acid sequence features were prespecified for analyses based on 1) being hypothesised to impact VE; and 2) having sufficient variability. Sieve analyses assessed VE by a single representative sequence and by viral population composition.

FINDINGS: The majority of Env features showed no evidence of differential VE, with only two signals having familywise error rate (FWER) P-values <0.10. In single-sequence analyses, VE declined with increasing physicochemical-weighted Hamming distance from the C97ZA vaccine insert in clade C broadly neutralising antibody resistance-associated signature positions (FWER P = 0.08). Sequence-predicted Env structural features showed no significant vaccine vs. placebo differences in structural divergence from the C97ZA vaccine-insert Env sequence. In multi-sequence analyses (median 121 sequences/individual), VE was higher against viral populations with ≥99% vs. <99% L832 prevalence (VE = 91.7%; 95% CI, 67.4-97.9 vs. VE = -7.0%; 95% CI, -55.5 to 26.4) (unadjusted P = 0.0002 for differential VE, FWER P = 0.023).

INTERPRETATION: Despite extensive prespecified and exploratory analyses including Env features supported by prior studies to potentially impact VE, there was only limited, weak evidence that Env sequence features modified VE in HVTN 705. Although previous work suggested a protective role of IgG3 binding to V1V2 in a small subgroup of vaccine recipients, a V1V2 sieve signal was absent.

FUNDING: National Institutes of Health and Johnson & Johnson.},
}

@article {pmid42673960,
year = {2026},
author = {Zambidis, AE and Siddaramaiah, LK and Gray, M and Konecny, AJ and Prlic, M},
title = {CaptureBody enables accurate unmixing for spectral flow cytometry.},
journal = {Cell reports methods},
volume = {},
number = {},
pages = {101571},
doi = {10.1016/j.crmeth.2026.101571},
pmid = {42673960},
issn = {2667-2375},
abstract = {Accurate spectral unmixing is a critical step for flow cytometry data analysis and requires a single stain control for every fluorescent parameter used in an experiment. Currently, compensation/unmixing particles are often used for making single stain controls when a target protein is of low abundance or a cell type is of low frequency. However, compensation/unmixing particles introduce incongruencies in emission spectra, compared to cells, resulting in spectral unmixing or compensation errors. To enable the use of cells regardless of the abundance of target proteins or immune cell type, we generated a bispecific antibody that links a human anti-CD45 and mouse anti-immunoglobulin G (IgG) variable region. We refer to this bispecific tool as CaptureBody (CB) and highlight the benefits of its final nanobody-based design. We provide all sequences and methods necessary for the in-house expression of a CaptureBody in order to disseminate their use for spectral flow cytometry experiments.},
}

@article {pmid42674547,
year = {2026},
author = {Fourment, M and Gao, J and Suchard, MA and Iv, FAM},
title = {Assessing the Validity of the Fixed Tree Topology Assumption in Phylodynamic Inference.},
journal = {Systematic biology},
volume = {},
number = {},
pages = {},
doi = {10.1093/sysbio/syag069},
pmid = {42674547},
issn = {1076-836X},
abstract = {Fixed tree topologies are widely used in phylodynamic analyses to reduce computational burden, yet the consequences of this assumption remain insufficiently understood. Here, we systematically assess the impact of various fixed-topology strategies on phylogenetic and phylodynamic parameter estimates across a diverse set of viral datasets. We compare fully Bayesian joint inference with fixed-topology strategies, including conditioning on maximum likelihood trees subsequently dated with LSD or TreeTime. Our analyses show that global parameters of the substitution and site models are largely robust to the fixed-topology assumption, whereas parameters that depend on the temporal structure of the tree, such as molecular clock rates, node ages, and demographic histories, can exhibit substantial systematic differences in their estimates. We do treat unconstrained Bayesian analyses as the reference, although we recognize that these too are model-based approximations. Nevertheless, our results highlight serious discordance associated with fixing the topology and underscore the need for faster, time-aware methods that simultaneously integrate topology and parameter estimation. These findings raise important questions about the balance between computational efficiency and inferential accuracy in phylodynamic studies. phylodynamic, tree topology, Bayesian inference, BEAST.},
}

@article {pmid42675051,
year = {2026},
author = {Hansen, DK and Dima, D and Mian, H and Devos, J and Brazauskas, R and Oloyede, T and Afrough, A and Ahmed, N and Anderson, LD and Banerjee, R and Berdeja, JG and Bidikian, A and Dhakal, B and Dias, A and Efebera, Y and Faisal, MS and Gowda, L and Hashmi, H and Mirza, AS and Mohan, M and Narra, R and Rosko, AE and Schroeder, M and Nishihori, T and Landau, H and Usmani, S and Pasquini, MC and Akhtar, OS and Sidana, S and Patel, KK},
title = {Correction: Safety and efficacy of ciltacabtagene autoleucel for relapsed/refractory multiple myeloma: a CIBMTR study.},
journal = {Blood cancer journal},
volume = {16},
number = {1},
pages = {},
doi = {10.1038/s41408-026-01605-9},
pmid = {42675051},
issn = {2044-5385},
}

@article {pmid42664501,
year = {2026},
author = {Bashey, A and Lee, SJ and Devine, SM and Shaw, BE and Dehn, JG and Pidala, JA and Hogan, WJ},
title = {Umbilical Cord Blood Donor Outcomes in BMTCTN1702.},
journal = {Blood advances},
volume = {},
number = {},
pages = {},
doi = {10.1182/bloodadvances.2026021835},
pmid = {42664501},
issn = {2473-9537},
}

@article {pmid42664960,
year = {2026},
author = {Yuan, D and Li, S and Zhang, R and Ng, RH and Su, Y and Lan, L and Shome, M and Smith, B and Troisch, P and Xie, J and Choi, J and Edmark, R and Chen, D and Rowen, L and Nguyen, A and Liu, R and Gutierrez, V and Brennan, C and McKasson, M and Murray, K and Wallick, JA and Algren, HA and Duven, A and Piening, B and Thomas, W and Kueh, HY and Magis, AT and Hadlock, J and Snyder, M and Goldman, JD and Heath, JR},
title = {A distinct effector B cell population drives autoantibody production in SARS-CoV-2 infection.},
journal = {Immunity},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.immuni.2026.08.002},
pmid = {42664960},
issn = {1097-4180},
support = {R01 CA264090/CA/NCI NIH HHS/United States ; },
abstract = {Autoantibodies (autoAbs) are linked to mortality and Long COVID, yet their cellular origins remain unclear. We analyzed the INCOV cohort and identified 12 age- and sex-matched participants with varying autoAb abundance and integrated single-cell RNA-seq and ATAC-seq data from B cells, plasma proteomics, proteome-wide autoAb profiling, clinical data, and in vitro assays. AutoAb abundance inversely correlated with neutralizing IgG and declined as infection resolved, paralleling the contraction of atypical memory B cells (AtMs). In vitro, AtMs preferentially differentiated into autoAb-producing antibody-secreting cells upon TLR7/8 stimulation. CD11c[+] AtMs (double-negative 2, DN2s) in autoAb-high individuals exhibited increased TLR7 signaling, oxidative stress, and isotype switching, regulated by transcription factors T-bet and XBP1. Integrated genetic and genomic analyses showed that DN2s had the strongest enrichment for autoimmune trait heritability and inferred regulatory effects of autoimmune risk variants among B cell subsets. These findings identify DN2s as key precursors of autoAb-producing cells during SARS-CoV-2 infection.},
}

@article {pmid42665019,
year = {2026},
author = {Amin, MK and Shahzad, M and Gandicheruvu, H and Noor, N and Khan, U and Kasaeian, A and Rukh, S and Abdelhakim, H and Lakkaraja, M and Hamadani, M and McGuirk, J and Mushtaq, MU},
title = {Impact Of Conditioning Intensity on Outcomes After Unrelated Donor Hematopoietic Cell Transplantation Using Post-Transplant Cyclophosphamide-Based GVHD Prophylaxis.},
journal = {Transplantation and cellular therapy},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.jtct.2026.08.050},
pmid = {42665019},
issn = {2666-6367},
}

@article {pmid42660882,
year = {2026},
author = {Chun, J and Tripathi, P and Flores-Garcia, Y and Madan, B and Lee, GA and Fahad, AS and Lei, H and Teng, IT and Hurlburt, NK and Flynn, BJ and Pancera, M and Miura, K and Zhou, T and Idris, AH and Zavala, F and Seder, RA and Kwong, PD and DeKosky, BJ},
title = {Anti-malaria antibody engineering broadens recognition motifs and reveals new homotypic interactions that enhance protective breadth.},
journal = {Nature communications},
volume = {17},
number = {1},
pages = {},
pmid = {42660882},
issn = {2041-1723},
support = {R01 AI181684/AI/NIAID NIH HHS/United States ; DP5 OD023118/OD/NIH HHS/United States ; R01AI192975//U.S. Department of Health & Human Services | National Institutes of Health (NIH)/ ; R01AI181684//U.S. Department of Health & Human Services | National Institutes of Health (NIH)/ ; R01 AI192975/AI/NIAID NIH HHS/United States ; DP5OD023118//U.S. Department of Health & Human Services | National Institutes of Health (NIH)/ ; },
mesh = {*Plasmodium falciparum/immunology/genetics ; *Protozoan Proteins/immunology/genetics/metabolism ; *Antibodies, Monoclonal/immunology/genetics ; Animals ; *Antibodies, Protozoan/immunology/genetics/chemistry ; Protein Engineering ; *Malaria, Falciparum/prevention & control/immunology/parasitology ; Antibody Affinity ; Humans ; Cryoelectron Microscopy ; Malaria Vaccines/immunology ; },
abstract = {The monoclonal antibody L9 mediates high-level protection against malaria in children for up to 6 months in Africa. L9 preferentially binds with high affinity to a triplicate of NVDP-minor repeats on the P. falciparum circumsporozoite protein (PfCSP). Here, we sought to improve the affinity of L9 to enhance protection against rare strains with two spatially separated minor repeats or a single minor repeat. Site saturation mutagenesis and yeast display-screening identified a panel of affinity-improved variants. In vivo challenge showed one variant, L9_yd19, to be modestly more potent against a transgenic Plasmodium encoding chimeric CSP with two widely spaced minor repeats from a Kenyan parasite strain, with no loss in potency against the benchmark 3D7 strain with its standard complement of minor repeats. L9_yd19 also had high affinity against NANP-major repeats and was protective against transgenic Plasmodium expressing CSP with a NANP12 knock-in lacking NVDP. Cryo-EM studies revealed L9_yd19 to recognize PfCSP with two distinct homotypic interfaces, which combined to yield two trimeric layers of antibodies comprising asymmetric trimers that dimerized in a head-to-head fashion. These data reveal a new antibody mechanism that utilizes interfaces involving dual homotypic symmetry elements, a 2-fold and an asymmetric 3-fold, for improved malaria prevention.},
}

*Plasmodium falciparum/immunology/genetics
*Protozoan Proteins/immunology/genetics/metabolism
*Antibodies, Monoclonal/immunology/genetics
Animals
*Antibodies, Protozoan/immunology/genetics/chemistry
Protein Engineering
*Malaria, Falciparum/prevention & control/immunology/parasitology
Antibody Affinity
Humans
Cryoelectron Microscopy
Malaria Vaccines/immunology

@article {pmid42649984,
year = {2026},
author = {Ch'en, PY and Zhang, Y and Hippe, DS and Bhakuni, R and Akaike, T and Hall, ET and Nghiem, P},
title = {Minimal Efficacy of Single-Agent Anti-PD-(L)1 Re-Exposure in Anti-PD-(L)1-Refractory Merkel Cell Carcinoma: A Retrospective Cohort Study of 16 Patients.},
journal = {Cancers},
volume = {18},
number = {16},
pages = {},
pmid = {42649984},
issn = {2072-6694},
support = {P01 CA225517/CA/NCI NIH HHS/United States ; P30 CA015704/CA/NCI NIH HHS/United States ; //MCC Patient Gift Fund at the University of Washington/ ; //Kelsey Dickson Team Science Courage Research Award: Advancing New Therapies for Merkel Cell Carcinoma/ ; },
abstract = {Background/Objectives: Anti-PD-(L)1 immune checkpoint inhibitors (ICIs) provide durable responses in nearly 50% of patients with advanced Merkel cell carcinoma (MCC). However, for those progressing on first-line ICI therapy, optimal subsequent therapy remains unclear. Although presumed to have limited benefit, the efficacy of re-exposure with anti-PD-(L)1 alone has not been formally reported. We assessed real-world outcomes of patients within a Seattle-based MCC repository who received this salvage approach. Methods: Among 106 patients who received salvage therapy after first-line ICI progression, 16 underwent single-agent anti-PD-(L)1 monotherapy re-exposure during salvage. Patients progressing >3 months after their last immunotherapy dose were excluded. Outcomes included progression-free survival (PFS), disease-specific survival (DSS), and objective response rate (ORR). Results: The median time from end of first-line ICI therapy to anti-PD-(L)1 re-exposure was 51 days (IQR 22-92). Most patients switched between PD-1 and PD-L1 inhibitors (n = 9), while others were re-exposed with the same agent (n = 5) or a different PD-1 inhibitor (n = 2). One of 16 patients experienced a partial response with the same PD-1 inhibitor (ORR 6%; 95% CI: 0.2-30%) at 3 months after re-exposure, followed by progression 10 months after re-exposure. Median PFS was 2.2 months (95% CI: 1.3-5.1 months), and median DSS was 14.7 months (95% CI: 10.4-NR). Conclusions: These data suggest that re-exposure with anti-PD-(L)1 monotherapy confers minimal and short-lived benefit in ICI-refractory MCC, reinforcing the need to develop alternative salvage strategies. Future trials for ICI-refractory MCC mandating an ICI monotherapy arm are unlikely to be appealing to patients or physicians based on a low chance of clinical benefit for this approach.},
}

@article {pmid42658506,
year = {2026},
author = {Boiko, JR and Carpenter, PA},
title = {Shuffling the JAKs: playing a new card in chronic GVHD.},
journal = {Blood advances},
volume = {10},
number = {17},
pages = {5834-5835},
pmid = {42658506},
issn = {2473-9537},
}

@article {pmid42658792,
year = {2026},
author = {Stansfield, SE and Moore, M and Boily, MC and Hughes, JP and Donnell, D and Bekker, LG and Dimitrov, DT},
title = {Estimated benefits of providing on-demand pre-exposure prophylaxis options for cisgender women in South Africa: A modeling study.},
journal = {PloS one},
volume = {21},
number = {8},
pages = {e0357094},
pmid = {42658792},
issn = {1932-6203},
support = {R01 AI179417/AI/NIAID NIH HHS/United States ; },
mesh = {Humans ; Female ; *Pre-Exposure Prophylaxis/methods ; South Africa ; *Anti-HIV Agents/therapeutic use/administration & dosage ; *HIV Infections/prevention & control ; Tenofovir/therapeutic use/administration & dosage ; Emtricitabine/therapeutic use ; Adult ; Male ; },
abstract = {INTRODUCTION: On-demand oral tenofovir disoproxil fumarate-emtricitabine (TDF/FTC) pre-exposure prophylaxis (PrEP) has been shown to be effective at preventing HIV acquisition among cisgender men and transgender women but is not recommended for cisgender women. On-demand PrEP may improve PrEP uptake, effective use, and persistence in cisgender women. We utilized published oral PrEP adherence-efficacy curves and data from HPTN 067 study to estimate effectiveness of different non-daily PrEP options when used by cisgender women and investigate which sub-groups may benefit most from on-demand PrEP.

METHODS: We created a synthetic cohort of PrEP users with data on sex act frequency and pill taking from the HPTN 067 Cape Town site. We simulated PrEP use with three PrEP regimens tested in HPTN 067: daily, time-driven (2 pills/week+1 pill after sex), and event-driven (1 pill before+1 pill after sex) PrEP, and hypothesized 2-1-1 PrEP (2 pills before+1 pill each of the two days after sex) for six months each. We estimated PrEP effectiveness based on the number of pills taken around sex acts. Adherence to 2-1-1 PrEP, which was not tested in the HPTN 067, was informed by observed adherence to event-driven PrEP. Assignment to 2-1-1 PrEP based on daily PrEP adherence and sex act frequency was also analyzed.

RESULTS: We estimated median effectiveness of 86% for daily, 47% for time-driven, 42% for event-driven, and 57% for 2-1-1 PrEP. PrEP users with low adherence to daily PrEP (less than 2.8 pills per week) benefited most from on-demand PrEP. In this subgroup, comprising 8% of the cohort, PrEP effectiveness increased from 41% to 44% when switching from daily to 2-1-1 PrEP while pill taking decreased from 2.2 to 1.4 pills per week; population-level effectiveness was unchanged when this subgroup switched to on-demand PrEP. We found no advantage in assigning 2-1-1 PrEP by sex act frequency.

CONCLUSIONS: Our model suggests that on-demand PrEP could benefit women with low daily PrEP adherence by decreasing the number of days when pills need to be taken and modestly increasing effectiveness compared to a daily regimen. This would be a valuable and easy-to-implement additional option in places where daily oral PrEP is already available.},
}

Humans
Female
*Pre-Exposure Prophylaxis/methods
South Africa
*Anti-HIV Agents/therapeutic use/administration & dosage
*HIV Infections/prevention & control
Tenofovir/therapeutic use/administration & dosage
Emtricitabine/therapeutic use
Adult
Male

@article {pmid42660114,
year = {2026},
author = {Nguyen, A and Heim, JB and Cordara, G and Chan, MC and Johannesen, H and Charlesworth, C and Li, M and Azumaya, CM and Madden, B and Krengel, U and Meves, A and Campbell, MG},
title = {Shared ligand-blocking mechanism but distinct conformational modulation by α5-targeting antibodies BIIG2 and MINT1526A.},
journal = {Structure (London, England : 1993)},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.str.2026.08.001},
pmid = {42660114},
issn = {1878-4186},
abstract = {Integrins are heterodimeric receptors important for cell adhesion and signaling. Integrin α5β1 is a key mediator of angiogenesis and its dysregulation is associated with tumor progression and metastasis. Despite numerous efforts, α5β1-targeting therapeutics have been unsuccessful due to poor efficacy and off-target effects. A contributing factor is our limited understanding of how integrin conformation influences interactions with therapeutics. Using cell-based functional assays, patient-derived xenografts, biophysics, X-ray crystallography, and electron microscopy, we shed light on these relationships by characterizing two anti-α5β1 antibodies, BIIG2 and MINT1526A. We show that both antibodies bind α5β1 with nanomolar affinity, reduce tube formation in vitro, and bind overlapping epitopes that block fibronectin binding. However, using electron microscopy, we reveal that while BIIG2 binding does not substantially alter the conformational states, MINT1526A preferentially recognizes the bent conformation and restricts the conformational ensemble. These insights can guide which aspects to prioritize to improve the design of future integrin-targeted therapeutics.},
}

@article {pmid42647771,
year = {2026},
author = {Ohlsen, TJD and Fredman, G and Burgara, J and Karvonen, KA and Gramatges, MM and Chow, EJ and Jones, SMW and Desai, AD},
title = {Development of a Pediatric Oncology Financial Toxicity Outcome Measure With Content and Face Validity: The Parent-Reported Instrument of Costs and Experiences (PRICE).},
journal = {JCO oncology practice},
volume = {},
number = {},
pages = {OP2600655},
doi = {10.1200/OP-26-00655},
pmid = {42647771},
issn = {2688-1535},
abstract = {PURPOSE: To address a lack of validated outcome measures of financial toxicity in pediatric oncology settings, we developed a novel caregiver-reported instrument.

METHODS: We first conducted qualitative concept elicitation interviews with family caregivers, then drafted de novo survey items guided by salient content domains. Items were reviewed by an expert panel who provided numeric ratings of item relevance to calculate content validity index (CVI), along with feedback on clarity and content. Items were removed or revised through a consensus process, organized into a preliminary measure, and forward- and back-translated to Spanish. We pretested items with caregivers in English and Spanish through iterative rounds of language-concordant cognitive interviews, revising between rounds to optimize comprehension, decision/response processes, and flow.

RESULTS: Concept elicitation with 21 caregivers (47% college-educated, 14% in Spanish) informed creation of 56 initial items across five content domains. CVI was <0.75 for 13 items; 12 were removed and one revised based on feedback. Of 43 items with CVI ≥0.75, eight were removed based on feedback and/or overlap with highly rated items. Thirty-six remaining items were revised and/or removed over six rounds of cognitive interviews with 22 different caregivers (42% college-educated, 23% in Spanish), then organized into a provisional 28-item instrument. In the final round of cognitive interviews, participants reported appropriate content, clarity, and organization in both languages.

CONCLUSION: We developed a novel caregiver-reported instrument to assess financial toxicity in pediatric oncology settings, with content and face validity. Future quantitative testing will evaluate its psychometric properties and other dimensions of validity to facilitate practical use.},
}

@article {pmid42649201,
year = {2026},
author = {Awany, D and Ariefdien, DT and Mendelsohn, SC and Rozot, V and Mulenga, H and Nyangu, S and Tameris, M and Moloantoa, T and Katona, A and Maruri, F and Noor, F and Panchia, R and Hlongwane, K and Stanley, K and van der Heijden, YF and Hadley, K and Fiore Gartland, A and Innes, C and Brumskine, W and Dheda, K and Jaumdally, S and Perumal, T and Martinson, N and Leslie, A and Fourie, B and Hiemstra, A and Malherbe, ST and Walzl, G and Naidoo, K and Churchyard, G and Chegou, NN and Sterling, TR and Hatherill, M and Scriba, TJ and , },
title = {Inflammatory biomarkers of asymptomatic and symptomatic tuberculosis.},
journal = {Nature communications},
volume = {17},
number = {1},
pages = {},
pmid = {42649201},
issn = {2041-1723},
support = {OPP1137034//Bill and Melinda Gates Foundation (Bill & Melinda Gates Foundation)/ ; },
mesh = {Humans ; *Biomarkers/blood ; *Tuberculosis/diagnosis/blood/immunology/genetics ; Proteomics ; Interferon-gamma/blood ; Transcriptome ; *Inflammation/blood ; Female ; Mycobacterium tuberculosis ; South Africa ; Male ; Gene Expression Profiling ; Asymptomatic Infections ; Adult ; },
abstract = {A large proportion of individuals with tuberculosis (TB) are asymptomatic. The biological and inflammatory underpinnings of asymptomatic TB are unknown and may differ from symptomatic TB. We characterise blood transcriptomic and proteomic profiles in South African community screening vs. health facility-based triage cohorts. Asymptomatic TB shares core transcriptomic and proteomic features with symptomatic TB, including upregulation of innate, interferon and inflammatory pathways and downregulation of T and B cell pathways. Integration of transcriptomic and proteomic data from asymptomatic TB individuals identifies two distinct sub-clusters characterized by higher or lower bacterial burden, blood IFN-γ responses, BMI, and chest radiographic abnormalities, suggesting different disease severity. We identify a new blood transcriptomic signature of asymptomatic TB. However, diagnostic performance of transcriptomic and proteomic markers is weaker for asymptomatic TB than symptomatic TB, suggesting that policy development for community-based, asymptomatic TB screening should not adopt biomarkers developed for symptomatic TB triage without further optimization.},
}

Humans
*Biomarkers/blood
*Tuberculosis/diagnosis/blood/immunology/genetics
Proteomics
Interferon-gamma/blood
Transcriptome
*Inflammation/blood
Female
Mycobacterium tuberculosis
South Africa
Male
Gene Expression Profiling
Asymptomatic Infections
Adult

@article {pmid42641160,
year = {2026},
author = {Hamilton, BK and Lee, CJ and Mattila, D and El-Jawahri, A and Cusatis, RN and Brazauskas, R and Sung, AD and Phelan, R and Horowitz, MM and Lee, SJ},
title = {Patient-Reported Outcomes in Clinical Trials: Lessons from the Blood and Marrow Transplant Clinical Trials Network.},
journal = {Blood advances},
volume = {},
number = {},
pages = {},
doi = {10.1182/bloodadvances.2026021114},
pmid = {42641160},
issn = {2473-9537},
abstract = {The Blood and Marrow Transplant Clinical Trials Network performs multi-center Phase 2 and Phase 3 clinical trials and has incorporated patient reported outcome (PRO) measures into study protocols since its inception. As with clinical data, collection and analysis of this type of information requires rigor to allow valid conclusions. This paper summarizes our experience with PROs over the last 25 years and reports on the quality of PRO reporting as well as lessons learned in this academic network setting.},
}

@article {pmid42641497,
year = {2026},
author = {Molin, K and Li, S and Barry, N and Ong, JSL and Iravani, A and Hofman, MS and Hassan, GM and Ebert, MA and Kendrick, J},
title = {Pre-therapeutic PSMA PET Imaging Biomarkers Demonstrate Prognostic Value in Patients Undergoing [[177]Lu]Lu-PSMA Therapy: A Systematic Review and Meta-analysis.},
journal = {Clinical genitourinary cancer},
volume = {24},
number = {7},
pages = {102628},
doi = {10.1016/j.clgc.2026.102628},
pmid = {42641497},
issn = {1938-0682},
abstract = {INTRODUCTION: [[177]Lu]Lu-prostate-specific membrane antigen (PSMA) radioligand therapy can improve outcomes in patients with metastatic castration-resistant prostate cancer, though response is highly variable in clinical practice. We performed a systematic review and meta-analysis to evaluate the prognostic value of pre-therapeutic PSMA PET-derived imaging biomarkers to better inform patient selection for treatment.

METHODS: PubMed, EMBASE, Web of Science, and Scopus were searched from inception to December 2025 in accordance with PRISMA guidelines (PROSPERO CRD420251074879). Pre-therapeutic PSMA PET biomarkers of interest were the mean and maximum standardised uptake value (SUVmean and SUVmax), PSMA tumour volume (PSMA-TV), total lesional uptake (PSMA-TLU), and total lesional quotient (PSMA-TLQ). Outcomes were overall survival (OS), prostate-specific antigen progression-free survival, and 50% reduction in prostate-specific antigen levels (PSA50). Random-effects meta-analyses were performed, prioritising multivariable-adjusted effect estimates. Risk of bias was assessed using the Quality In Prognosis Studies tool.

RESULTS: Thirty-seven studies were included, with 33 contributing to quantitative synthesis (n = 2993). For each unit increase in SUVmean, there was a reduced risk of death (hazard ratio [HR] = 0.88, 95% CI, 0.85-0.92; P < .001) and PSA progression (HR = 0.870, 95% CI, 0.761-0.995; P = .042), along with higher odds of PSA50 response (odds ratio = 2.12, 95% CI: 1.20-3.74; P = .010). Higher PSMA-TV was associated with poorer OS. Composite metrics were prognostic, with PSMA-TLQ demonstrating stronger associations with survival than PSMA-TLU. SUVmax showed limited prognostic value. Most studies were retrospective and were classified as having moderate risk of bias.

CONCLUSION: Baseline PSMA PET-derived biomarkers provide relevant prognostic information and may complement established clinical biomarkers to support risk stratification and patient selection for [[177]Lu]Lu-PSMA therapy.},
}

@article {pmid42641934,
year = {2026},
author = {Sasamoto, N and Shafrir, AL and Sieberg, CB and Vitonis, AF and Lin, N and DePari, M and Till, S and DiVasta, AD and Garbutt, K and Vincent, K and Becker, C and Zondervan, KT and Terry, KL and Missmer, SA},
title = {Endometriosis risk factors and comorbidities by endometriosis lesion macrophenotypes: An analysis from the What is Endometriosis (WisE) study.},
journal = {American journal of obstetrics and gynecology},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.ajog.2026.08.026},
pmid = {42641934},
issn = {1097-6868},
abstract = {BACKGROUND: While endometriosis is thought to be a heterogeneous disease, the pathophysiologic heterogeneity across the three visualized lesion macrophenotypes (i.e., superficial peritoneal endometriosis(SPE) lesions, endometriomas, and deep lesions) remains unclear.

OBJECTIVES: This study aimed to investigate associations between known and putative risk factors and co-existing comorbidities with odds of endometriosis lesion macrophenotypes.

STUDY DESIGN: We conducted a pooled, cross-sectional analysis using data from 1,244 participants surgically diagnosed with endometriosis and 1,271 without endometriosis who participated in three World Endometriosis Research Foundation Endometriosis Phenome and Biobanking Harmonization Project compliant population-based studies from North America and Europe. Multivariable logistic regression models adjusting for age at questionnaire completion and studies were used to calculate odds ratios (OR) and 95% confidence intervals (CI) for the associations between participant characteristics of known and putative risk factors and co-existing comorbidities and surgically-confirmed endometriosis. Polytomous logistic regression was used to examine the associations among case groups defined by endometriosis macrophenotype, with likelihood ratio tests used to evaluate statistically significant differences between macrophenotypes presented as p-heterogeneity (p-het).

RESULTS: Among endometriosis cases, 834(71%) had SPE only, 92(8%) had at least one endometrioma, 129(11%) had deep lesions, and 111(10%) had both endometrioma and deep lesions. Younger age at menarche was associated with significantly higher odds for having SPE only and deep+endometrioma macrophenotypes (≤11 vs. 12 years-old, OR=1.29, CI=1.01-1.65 and OR=2.07, CI=1.11-3.86, respectively), but not associated with endometrioma or deep lesions alone (p-heterogeneity=0.05). Presence of chronic overlapping pain conditions was associated with greater odds of endometriosis overall (OR=1.66, CI=1.49-1.85 per condition) and of SPE only(OR=1.80, CI=1.59-2.04 per condition) and deep lesions(OR=1.76, CI=1.44-2.15 per condition), but not with macrophenotypes including endometrioma(p-het=0.0001). Unsupervised clustering by risk factors and co-existing conditions showed distinct associative patterns by surgically-visualized lesion macrophenotypes.

CONCLUSIONS: These results showing heterogeneity of individual risk factors and co-existing conditions across endometriosis macrophenotypes support the concept that endometriosis macrophenotypes may have different etiologies and underscores the importance of evaluating risk factors and biomarkers by endometriosis lesion macrophenotypes.},
}

@article {pmid42643813,
year = {2026},
author = {Liu, J and Zhang, N and An, Z and Heczey, A},
title = {Interleukin-15-armored ALPPL2 CAR T cells demonstrate robust preclinical efficacy for solid tumors.},
journal = {Molecular therapy. Oncology},
volume = {34},
number = {3},
pages = {201319},
pmid = {42643813},
issn = {2950-3299},
}

@article {pmid42644818,
year = {2026},
author = {Robertson, DJ and Dominitz, JA and Beed, A and Boardman, K and Del Curto, BJ and Guarino, PD and Huang, GD and Imperiale, TF and LaCasse, A and Larson, M and Gupta, S and Lieberman, D and Planeta, B and O'Leary, TJ and Shaukat, A and Sultan, S and Kyriakides, TC and , },
title = {Race, ethnicity, and prior colorectal screening test use in CONFIRM colonoscopy vs fecal immunochemical testing trial participants.},
journal = {JNCI cancer spectrum},
volume = {},
number = {},
pages = {},
doi = {10.1093/jncics/pkag080},
pmid = {42644818},
issn = {2515-5091},
abstract = {BACKGROUND: Colorectal cancer (CRC) outcomes vary by both race and ethnicity, and screening test use may contribute to this variation. We examined the association of race, ethnicity, and associated factors with CRC screening test use in a setting where financial barriers to screening are mitigated.

METHODS: Survey information was gathered from US Veteran participants (N = 50,125) when enrolled into a randomized trial comparing screening colonoscopy to annual fecal immunochemical testing (FIT) in the prevention of CRC mortality. The primary exposures of interest were the participants' self-identified race and ethnicity, with adjustment for variables capturing access to care. Multivariable logistic regression, stratified by site and age, was used to assess the relationship between exposures of interest and prior use of any CRC screening test, prior colonoscopy, and prior fecal occult blood test (FOBT, including FIT) use.

RESULTS: Screening test use was common (N = 28,330, 56.5%) with more Veterans reporting prior FOBT (N = 20,386, 40.7%) than prior colonoscopy (N = 12,671, 25.3%). In multivariable analysis, Black participants were more likely (odds ratio (OR), 1.06; 95% confidence interval (CI) 1.01-1.12) to have had any prior screening relative to White persons and this finding was driven by more frequent FOBT use relative to White persons (OR, 1.16; 95% CI 1.10-1.23). There was no association between Hispanic ethnicity (relative to White persons) on the primary outcomes.

CONCLUSIONS: In this cohort, prior screening test use was common, with observed variation in overall test use by race, but not ethnicity. Further study of CRC screening test use in diverse populations are needed.

CLINICALTRIALS.GOV ID: NCT#05612347.},
}

@article {pmid42640567,
year = {2026},
author = {Hardikar, S and Gigic, B and Kresovich, JK and Damerell, V and Himbert, C and Ose, J and Toriola, AT and Shibata, D and Li, CI and Figueiredo, JC and Byrd, DA and Siegel, EM and Kahlert, C and Brobeil, A and Schirmacher, P and Ulrich, CM and Barrow, TM},
title = {Epigenetic aging of colorectal mucosa in cancer development.},
journal = {Journal of the National Cancer Institute},
volume = {},
number = {},
pages = {},
doi = {10.1093/jnci/djag297},
pmid = {42640567},
issn = {1460-2105},
abstract = {BACKGROUND: The past decade has seen the development of epigenetic models of aging that accurately estimate chronological age and predict disease incidence and mortality. These estimates are modulated by lifestyle and environmental factors linked to carcinogenesis, but to date this has primarily been studied in blood.

METHODS: We examined epigenetic aging in normal colonic tissue (n = 96), adjacent mucosa (n = 245) and tumors (n = 208), using models trained on age (Horvath, Hannum, Zhang), mortality (PhenoAge, GrimAge), aging rate (DunedinPACE), cellular mitotic history (EpiTOC, epiTOC2, miAGe), and telomere length (DNAmTL).

RESULTS: The Horvath model was the most accurate estimator of chronological age in normal colonic mucosa, with high correlation (r > 0.70) between the Horvath, Hannum, Zhang, PhenoAge and GrimAge models, and between mitotic clocks (r > 0.94). All models showed similar performance in normal tissue and adjacent mucosa, but substantially more variation in estimates in tumors. Significant differences in age acceleration were present between normal and adjacent mucosa by six models (Hannum, Zhang, PhenoAge, EpiTOC, epiTOC2 and miAge), while tumors showed highly significant differences by all models. Age acceleration differed by region of the colon, with varying patterns by model type. Physical activity (PhenoAge), smoking history (GrimAge), and alcohol consumption (Horvath, mitotic clocks) were associated with epigenetic aging in adjacent mucosa, while smoking history, smoking intensity, and alcohol consumption were associated with DNAmTL in tumors.

CONCLUSIONS: Our study reveals an impact of tissue type, region, and lifestyle factors on epigenetic aging, but also highlights significant heterogeneity between models and the need for careful consideration within study design.},
}

@article {pmid42640721,
year = {2026},
author = {Dhodapkar, KM and Matera, A and Duffy, AM and Taz, A and Manalo, RJ and Yushak, M and Kuchadkar, R and Lawson, DH and Dhodapkar, MV},
title = {B-cell depletion improves therapeutic index of combination checkpoint blockade in patients with advanced melanoma.},
journal = {The Journal of clinical investigation},
volume = {},
number = {},
pages = {},
doi = {10.1172/JCI205606},
pmid = {42640721},
issn = {1558-8238},
abstract = {BACKGROUND: Combined checkpoint blockade (CCB) of programmed-death-1 (PD-1) and cytotoxic-T-lymphocyte-associated protein-4 (CTLA-4) is highly active in melanoma but limited by significant morbidity from immune-related adverse events (irAEs). Effective strategies to prevent CCB-mediated irAEs are lacking.

METHODS: Patients with advanced melanoma were randomly assigned to receive standard of care ipilimumab and nivolumab alone (Arm-A: ipi/nivo, n=7) or with one cycle of rituximab (Arm-B; ipi/nivo+rituximab, n=7).

RESULTS: Patients receiving ipi/nivo+rituximab experienced lower rates of > grade-3(G3) irAEs (14% versus 57%) and superior G3-irAE-free survival compared to those in ipi/nivo arm (2-year G3-irAE-free survival 86% versus 29% (p=0.01), without adverse impact on tumor regression or survival. G3 hypersensitivity reactions to rituximab (43% in Arm-B) prompted trial closure. Rituximab depleted pre-therapy activated naïve B cells linked to autoimmunity and enhanced CCB-mediated induction of myeloid inflammation and CXCL13+ICOS+ CD4 T cells.

CONCLUSION: B-cell depletion favorably modulates CCB-mediated immune activation and may reduce irAE risk.

TRIAL REGISTRATION: ClinicalTrials.gov NCT03719131 Funding: NIH.},
}

@article {pmid42640729,
year = {2026},
author = {Moisoiu, V and Lourman, R and Szulzewsky, F and Kessler, T and Collotta, G and Porro, A and Bertolini, A and Singer, F and Cimino, PJ and Hertler, C and Wick, W and Reifenberger, G and Holland, EC and Sartori, AA and Weller, M and Wirsching, HG},
title = {Loss of MSH6 or MSH2 sensitizes progressive glioblastoma to radiotherapy.},
journal = {The Journal of clinical investigation},
volume = {},
number = {},
pages = {},
doi = {10.1172/JCI205299},
pmid = {42640729},
issn = {1558-8238},
}

@article {pmid42640961,
year = {2026},
author = {Melhorn, SJ and Valencia, AP and Schenk, JM and Garcia, JM and Beatty, SJ and Konchan, A and Brandao, AF and Acosta-Vega, NL and Marcinek, DJ and Tong, J and Neuhouser, ML and Schur, EA},
title = {Assessing the physiology of weight loss based on real-time weight monitoring: The ADAPT behavioral weight loss study protocol.},
journal = {PloS one},
volume = {21},
number = {8},
pages = {e0354678},
pmid = {42640961},
issn = {1932-6203},
support = {R01 DK134417/DK/NIDDK NIH HHS/United States ; K24 HL144917/HL/NHLBI NIH HHS/United States ; R01 DK089036/DK/NIDDK NIH HHS/United States ; P30 DK035816/DK/NIDDK NIH HHS/United States ; K01 HL164761/HL/NHLBI NIH HHS/United States ; R01 DK144233/DK/NIDDK NIH HHS/United States ; P30 DK017047/DK/NIDDK NIH HHS/United States ; },
mesh = {Adult ; Female ; Humans ; Male ; Middle Aged ; Diet, Reducing ; Exercise ; Monitoring, Physiologic/methods ; *Obesity/physiopathology/therapy ; *Weight Loss/physiology ; },
abstract = {Improving health outcomes via sustained weight loss and maintenance requires advancing understanding of the metabolic, appetitive, and neurological alterations that counteract-and eventually halt-weight loss. Prior studies have demonstrated increased appetite as well as metabolic adaptations, such as increased energy efficiency, in response to weight loss. However, previous study designs utilized experimentally determined weight loss plateaus and did not investigate spontaneously occurring plateaus nor study participants in their natural, free-living, environments during weight loss. The Assessing Diet, Appetite, and Physiology Throughout weight loss (ADAPT) study was designed to address these limitations of prior research and elucidate mechanistic factors involved in spontaneous cessation of intentional weight loss in humans. ADAPT enrolls participants with obesity who undergo behavioral weight loss via a reduced calorie diet and increased physical activity. Participants' daily weight is monitored remotely, and new analytic approaches identify weight-loss phases in real time so that study assessments can be targeted to each participants' individualized trajectory during dynamic weight loss. Deep phenotyping of participants includes anthropometric, metabolic, neurophysiologic, and behavioral assessments; physical activity and physiologic monitoring via wearable devices; and serial sampling of biological tissues such as blood, adipose tissue, and muscle. In summary, the ADAPT study design is generating a uniquely informative and integrative dataset for deepening understanding of the biological mechanisms that halt behaviorally-induced weight loss and thereby limit its long-term health benefits for patients with obesity. NCT06174389.},
}

Adult
Female
Humans
Male
Middle Aged
Diet, Reducing
Exercise
Monitoring, Physiologic/methods
*Obesity/physiopathology/therapy
*Weight Loss/physiology

@article {pmid42633301,
year = {2026},
author = {Kikawa, C and Huddleston, J and Turner, SA and Loes, AN and Liu, J and Gang, S and Griffiths, T and Drapeau, EM and Cowling, BJ and Ho, F and Leung, NHL and Englund, JA and Lacombe, K and Watanabe, S and Hasegawa, H and Busch, M and Lanteri, M and Stone, M and Spencer, B and Neher, RA and Smith, DJ and Bedford, T and Hensley, SE and Bloom, JD},
title = {Near real-time data on the human neutralizing antibody landscape to influenza virus as of early 2026 to inform vaccine-strain selection.},
journal = {Virus evolution},
volume = {12},
number = {1},
pages = {veag046},
pmid = {42633301},
issn = {2057-1577},
support = {75N93021C00014/OD/NIH HHS/United States ; P30 CA015704/CA/NCI NIH HHS/United States ; S10 OD028685/OD/NIH HHS/United States ; R01 AI165818/AI/NIAID NIH HHS/United States ; 75N93021C00015/OD/NIH HHS/United States ; S10 OD020069/OD/NIH HHS/United States ; F30 AI186284/AI/NIAID NIH HHS/United States ; },
abstract = {Twice each year, a decision is made on whether to update the strains included in the seasonal influenza vaccine to better match the most recent circulating viral strains. To characterize the antigenic properties of current seasonal influenza A strains to inform the upcoming decision about which strains to include in the 2026-7 Northern Hemisphere vaccine, here we perform high-throughput sequencing-based neutralization assays using a library of 57 H3N2 and 34 H1N1 influenza hemagglutinins reflecting the circulating diversity of strains in late 2025 to early 2026. We assay this library against 302 human sera collected in late 2025. The resulting data set encompasses 27 409 titres and provides a near real-time portrait of the human neutralizing antibody landscape against influenza virus. We find that many human sera have lower titres against the K subclade of H3N2 and the D.3.1.1 subclade of H1N1; these subclades have recently become dominant among their respective subtypes. Our measurements also reveal variability in titres to different subvariants within the K subclade of H3N2, with titres especially low to subclade K strains with additional mutations in antigenic regions D and E. We make all our data and accompanying visualizations publicly available to enable their use in vaccine-strain selection and analyses of influenza evolution and immunity.},
}

@article {pmid42636676,
year = {2026},
author = {Ford, E},
title = {Resilience to Disaster: System Design and Future Directions.},
journal = {Seminars in radiation oncology},
volume = {39},
number = {},
pages = {151055},
doi = {10.1016/j.semradonc.2026.151055},
pmid = {42636676},
issn = {1532-9461},
abstract = {Rapid-onset disasters pose a particular challenge to oncology services, especially radiation oncology, which is highly technical and dependent on complex equipment and digital infrastructure. Thoughtful preparation can anticipate vulnerabilities and improve disaster response; however, recommendations are still emerging and individual clinics are largely left to develop and activate their own disaster preparedness plans. A principled conceptual framework for system design is therefore needed. In this article, we discuss such a framework, mapping disaster preparedness considerations onto the widely-used Donabedian model of healthcare quality, which evaluates care across 3 interdependent domains: Structure, Process, and Outcome. We draw on examples from outside oncology-including humanitarian surgical programs and institutional pandemic responses-that have applied this model at the clinical and operational level. We demonstrate that previously reported experience of disaster response in radiation oncology maps coherently onto this framework, and we present specific design principles and practical approaches that organizations can employ. Current guidance from professional societies and accreditation bodies is reviewed, and future directions-including formal risk assessment and commercial disaster-recovery solutions-are discussed. When thoughtfully applied, these principles of system design can help oncology programs build meaningful resilience before the next disaster arrives.},
}

@article {pmid42639030,
year = {2026},
author = {Shnorhavorian, M and Amory, JK and Schwartz, SM and Bhatia, S and Armenian, S and Grier, HE and Chow, EJ and Joshi, R and Beck, D and Skinner, MK},
title = {Weighted epigenetic site correlation network analysis of chemotherapy impacts on osteosarcoma cancer survivors' male fertility, sperm, and endocrine parameters.},
journal = {Environmental epigenetics},
volume = {12},
number = {1},
pages = {dvag029},
pmid = {42639030},
issn = {2058-5888},
support = {R01 CA175216/CA/NCI NIH HHS/United States ; U10 CA098543/CA/NCI NIH HHS/United States ; U10 CA180886/CA/NCI NIH HHS/United States ; UG1 CA189955/CA/NCI NIH HHS/United States ; },
abstract = {The impacts of chemotherapy exposure on adolescent male osteosarcoma survivors as adults were investigated using a number of physiological parameters, with a focus on chemotherapy, reproduction, and sperm. The Children's Oncology Group (COG) clinical sites (protocol ALTE16C1) of previously collected and stored sperm samples were obtained for this analysis. The epigenetic DNA methylation alterations in sperm were assessed in 176 control adult male patients' sperm, and 183 chemotherapy-exposed osteosarcoma survivors' adult male sperm were provided by COG sites. The current study used a weighted gene co-expression network analysis computational approach that was adopted for use as a weighted epigenetic site correlation network analysis. This analysis identified correlation coefficients between differential DNA methylation regions and other DNA methylation sites with physiological and chemotherapy parameters. Module-trait relationships in the data were determined for epigenetic modules, which highly correlated with sperm parameters, reproductive hormones, and several chemotherapies (e.g. cisplatin). Gene associations of these epigenetic sites were identified and correlated to chemotherapy-associated genes and pathways, as well as reproductive parameters. Observations demonstrate dramatic impacts of adolescent chemotherapy on later adult life sperm epigenetics. Clearly, epigenetics has the potential to mediate the actions of chemotherapy on later life physiology and may potentially impact future generations through epigenetic transgenerational inheritance mechanisms, but this needs further investigation.},
}

@article {pmid42639747,
year = {2026},
author = {Owens, L and Rizopoulos, D and Fainberg, J and Carlsson, S and Liso, N and McBride, S and Laudone, V and Etzioni, R and Taylor, JMG},
title = {Dynamic Predictions and Predictimands for Salvage Therapy in Recurrent Prostate Cancer Using Joint Models.},
journal = {Statistics in medicine},
volume = {45},
number = {20-22},
pages = {e70710},
pmid = {42639747},
issn = {1097-0258},
support = {R35 CA274442/CA/NCI NIH HHS/United States ; U01 CA253915/CA/NCI NIH HHS/United States ; },
mesh = {Humans ; Male ; *Prostatic Neoplasms/therapy/blood/pathology ; *Salvage Therapy/methods ; Prostate-Specific Antigen/blood ; *Neoplasm Recurrence, Local/therapy ; *Models, Statistical ; Survival Analysis ; Computer Simulation ; Longitudinal Studies ; Prediction Algorithms ; Biomarkers, Tumor/blood ; Monte Carlo Method ; },
abstract = {Prostate cancer patients with biochemical recurrence (BCR) face a decision of whether to start salvage therapy (ST), which may reduce the probability of metastatic progression at the cost of side effects. To inform the decision to start ST at or after BCR, models that make counterfactual predictions incorporating treatment are highly desirable. However, estimation of such models using observational data requires care due to time-varying confounding by the longitudinal biomarker prostate-specific antigen (PSA). Moreover, a careful definition of the estimands of interest, referred to as "predictimands", is required due to the possibility of delayed initiation of treatment after biochemical recurrence. In this study, we utilize the framework of joint longitudinal and survival models to tackle these issues, estimating a model for pre-ST PSA trajectories and risk of metastasis that incorporates the effect of ST, from a dataset of 2075 patients with BCR. We define relevant predictimands for a new patient after BCR under three scenarios: Immediately treated, never treated, and treatment under a dynamic regime, where ST is started when PSA is observed to exceed a pre-specified threshold. We propose a Monte Carlo scheme for computing these predictimands, adapting previous work on dynamic predictions from joint models to account for treatment timing. This methodology is applied to an example patient and validated in a simulation study. This methodology could be adapted to a wide variety of applications requiring counterfactual predictions in the presence of time-varying treatments and biomarkers. Code to implement such analyses is available in the R package JMbayes2.},
}

Humans
Male
*Prostatic Neoplasms/therapy/blood/pathology
*Salvage Therapy/methods
Prostate-Specific Antigen/blood
*Neoplasm Recurrence, Local/therapy
*Models, Statistical
Survival Analysis
Computer Simulation
Longitudinal Studies
Prediction Algorithms
Biomarkers, Tumor/blood
Monte Carlo Method

@article {pmid42348788,
year = {2026},
author = {Fries, C and Ji, L and Devidas, M and Rabin, KR and Loh, ML and Lee, LW and Kirsch, I and Teachey, DT and Gupta, S and Wood, BL and Rau, RE},
title = {Minimal residual disease by high-throughput sequencing in standard risk-favorable pediatric B-lymphoblastic leukemia.},
journal = {Blood advances},
volume = {10},
number = {17},
pages = {6027-6031},
doi = {10.1182/bloodadvances.2026020975},
pmid = {42348788},
issn = {2473-9537},
support = {U10 CA180886/CA/NCI NIH HHS/United States ; U10 CA180899/CA/NCI NIH HHS/United States ; U24 CA196173/CA/NCI NIH HHS/United States ; },
}

@article {pmid42619944,
year = {2026},
author = {Nakalega, R and Haines, D and Hayes, R and Eshleman, SH and Ayles, H and Bock, P and Floyd, S and Fidler, S and Clarke, W and Agyei, Y and Breaud, A and Gati, BM and Nakabiito, C and Donnell, D},
title = {Discordance Between Biomarker-Confirmed Antiretroviral Therapy and Self-Reported HIV Status Among People Living with HIV in Zambia and South Africa: A Secondary Analysis of HPTN 071 (PopART).},
journal = {medRxiv : the preprint server for health sciences},
volume = {},
number = {},
pages = {},
pmid = {42619944},
abstract = {BACKGROUND: Misclassification of HIV status in population-based surveys remains a critical barrier to accurate surveillance and program evaluation. Self-reported HIV status may diverge from objective measures, particularly among individuals receiving antiretroviral therapy (ART). We used biomarker-confirmed antiretroviral (ARV) drug detection to assess the prevalence and correlates of discordance between self-reported HIV status and biologic evidence of HIV treatment among people living with HIV (PLHIV) in Zambia and South Africa.

METHODS: We conducted a secondary analysis of the HPTN 071 (PopART) cluster-randomized trial. At the 24-month survey visit, participants underwent HIV testing and laboratory assessment for ARV drugs in plasma. We defined discordant self-report (hereafter "non-disclosure") as reporting HIV-negative or unknown status among individuals with ARV drugs detected. We estimated the prevalence of non-disclosure, compared prevalence by study arm, and used modified Poisson regression to identify associated factors. We also examined whether non-disclosure was associated with viral suppression (<400 copies/mL).

RESULTS: Among 3,240 PLHIV with ARV drugs detected, 552 (17.0%) did not report an HIV-positive status-indicating that nearly one in six individuals on ART were misclassified by self-report. Non-disclosure did not differ between intervention and control arms (adjusted relative risk [aRR]: 1.03; 95% CI: 0.67-1.58). Non-disclosure was more common among younger individuals (age 18-24 years: aRR 2.30; 95% CI: 1.66-3.19), men (aRR: 1.39; 95% CI: 1.07-1.79), and those in formal employment (aRR: 1.42; 95% CI: 1.06-1.90). Individuals reporting condomless sex at last encounter were also more likely not to disclose (aRR: 1.59; 95% CI: 1.31-1.92). Viral suppression was high overall (93.7%) and did not differ by disclosure status (aRR: 1.06; 95% CI: 0.74-1.52).

CONCLUSION: A substantial proportion of PLHIV receiving ART did not report a known HIV-positive status, highlighting important discordance between biomarker evidence and self-reported data. Despite high levels of viral suppression, these individuals remain "hidden" from routine surveillance, with implications for estimating HIV diagnosis and treatment coverage. Strategies that incorporate objective measures alongside self-report, and that address social and structural barriers to disclosure, are essential to improve the accuracy of HIV surveillance and guide effective public health responses.},
}

@article {pmid42627660,
year = {2026},
author = {Matrajt, L and Stansfield, SE and Moore, M and Donnell, DJ and Brown, ER and Cohen, MS and Dimitrov, D},
title = {Treatment as Prevention and HIV Transmission in the US.},
journal = {JAMA network open},
volume = {9},
number = {8},
pages = {e2630330},
pmid = {42627660},
issn = {2574-3805},
mesh = {Humans ; *HIV Infections/prevention & control/transmission/epidemiology/drug therapy ; United States/epidemiology ; Female ; Male ; Incidence ; Prevalence ; *Anti-HIV Agents/therapeutic use ; Adult ; },
abstract = {IMPORTANCE: Providing treatment to all people living with HIV (PLHIV), a strategy known as treatment as prevention, is a highly effective intervention against HIV. Policies that reduce access to antiretroviral therapy (ART), an important component of treatment-as-prevention (TasP) strategies, might undermine decades of HIV control in the US and result in thousands of new HIV infections.

OBJECTIVE: To estimate the association between TasP and the HIV epidemic in the US from 2011 to 2025 and to project the outcomes of a potential rollback of this policy.

In this decision analytical model, HIV incidence and prevalence from 2011 to 2030 were simulated. PLHIV were stratified by transmission group (men who have sex with men, heterosexual men, heterosexual women, and people who inject drugs) and stage of the HIV care cascade (undiagnosed, diagnosed but not receiving ART, receiving ART with detectable viremia, and receiving ART and virally suppressed).

EXPOSURE: Change in HIV care cascade.

MAIN OUTCOMES AND MEASURES: Annual HIV transmissions from 2011 to 2025 were compared with HIV care cascade (1) following the observed trend (with TasP) or (2) fixed at 2011 levels, without TasP. The impact of preexposure prophylaxis (PreP) rollout since 2017 was also estimated. Finally, HIV transmission from 2026 to 2030 was projected assuming that (1) 10% to 30% of PLHIV immediately lose ART access, reflecting the estimated share of ART funded through federal subsidies, (2) no change, or (3) a moderate increase in ART access.

RESULTS: In 2011, there were 1 008 300 PLHIV. In 2025, treatment as prevention was associated with an estimated 44.5% reduction in HIV incidence; PrEP, a 20.5% reduction; and treatment as prevention plus PrEP, a 61.8% reduction. From 2011 to 2025, TasP averted an estimated 197 400 new HIV acquisitions in the US, PrEP averted 33 200, and the 2 combined averted 293 200. Immediate losses of ART access affecting 10%, 20%, or 30% of treated PLHIV were associated with approximately 35 900, 81 700, and 111 200 additional HIV acquisitions between 2026 and 2030, respectively, substantially reversing the population-level gains achieved through TasP.

CONCLUSIONS AND RELEVANCE: In this decision analytical model estimating the potential effects of reductions in ART access, findings suggest that these reductions will not only jeopardize individual health outcomes and over a decade of progress toward HIV elimination but also result in thousands of new HIV acquisitions over the next 5 years.},
}

Humans
*HIV Infections/prevention & control/transmission/epidemiology/drug therapy
United States/epidemiology
Female
Male
Incidence
Prevalence
*Anti-HIV Agents/therapeutic use
Adult

@article {pmid42628293,
year = {2026},
author = {Mora, AM and Mejía-Arangure, JM and Dockerty, JD and Rashed, WM and Núñez-Enríquez, JC and Auvinen, A and Bailey, H and Bonaventure, A and Lee, PC and Chow, EJ and Clavel, J and Crowe, J and de Smith, AJ and Dolatkhah, R and Erdmann, F and Filippini, T and Force, LM and Hansen, J and Heck, JE and Infante-Rivard, C and Kane, E and Kang, AY and Kantzanou, M and Lohi, O and Lupo, PJ and Ma, X and Magnani, C and Marcotte, EL and Metayer, C and Nikkilä, A and Ntzani, E and Olsson, A and Petridou, ET and Pombo-de-Oliveira, MS and Psaltopoulou, T and Ribeiro, KB and Roman, E and Scott, R and Sergentanis, TN and Scheurer, ME and Schraw, JM and Schüz, J and Vinceti, M and Wiemels, J and Wünsch-Filho, V and Yang, T and Mueller, BA and Spector, LG},
title = {The Childhood Cancer and Leukemia International Consortium (CLIC): Expanding global collaboration in pediatric cancer etiology research.},
journal = {Cancer epidemiology},
volume = {104},
number = {},
pages = {103208},
doi = {10.1016/j.canep.2026.103208},
pmid = {42628293},
issn = {1877-783X},
support = {R01 CA266253/CA/NCI NIH HHS/United States ; },
mesh = {Humans ; Child ; *Leukemia/epidemiology/etiology ; *Neoplasms/etiology/epidemiology ; International Cooperation ; Female ; Registries ; },
abstract = {Childhood cancers are rare, but incidence has risen modestly in countries with robust registration, partly reflecting improved diagnosis. In high-income countries, cancer is the leading cause of disease-related death in children. Marked inequities in incidence, survival, and research capacity underscore the need for large-scale collaboration to identify environmental, genetic, and contextual determinants of risk. The Childhood Cancer and Leukemia International Consortium (CLIC) was established in 2007 to study the etiology of childhood leukemia and later expanded in 2019 to include other childhood cancers, principally solid tumors. CLIC pools harmonized, individual-level data from case-control and cohort studies, obtained through interviews, record linkage (insurance claims, registries), or geographic information systems, and integrates germline genomic data where available. Membership has grown from 13 studies in 9 countries to 57 studies in 21 countries; recruitment spans the early 1960s to the present and encompasses approximately 150,000 cases across all tumor types and 300,000 controls with clinical, demographic, and exposure data, centralized via harmonized data dictionaries at the Data Coordination Center, established in 2014 at the International Agency for Research on Cancer, and supported by a secure analysis platform. Pooled analyses across diverse populations have implicated parental age, prenatal vitamin or folic acid use, mode of delivery, fetal growth, selected congenital anomalies, occupational or household exposures (e.g., pesticides), paternal smoking, and markers of early-life immune modulation (e.g., breastfeeding, daycare attendance) in leukemia risk, informing carcinogen evaluation and prevention. The integration of genetic ancestry and germline susceptibility data is clarifying ancestry-related differences in leukemia biology and outcomes, while confirming risk loci with population-specific effects. CLIC is now adding polygenic risk scores and exposomic data to refine etiologic subtyping and identify modifiable pathways, while broadening representation from underserved regions through partnership-building and capacity-strengthening.},
}

Humans
Child
*Leukemia/epidemiology/etiology
*Neoplasms/etiology/epidemiology
International Cooperation
Female
Registries

@article {pmid42628582,
year = {2026},
author = {Till, C and Tangen, CM and Goodman, P and Unger, JM and Thompson, IM},
title = {No Evidence of Post-Finasteride Syndrome in 267,983 person-years follow-up in the Prostate Cancer Prevention Trial.},
journal = {Urology},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.urology.2026.08.020},
pmid = {42628582},
issn = {1527-9995},
abstract = {OBJECTIVE: To investigate Post-Finasteride Syndrome, a broad range of symptoms reported in case reports and case series among patients who have received finasteride, a five-alpha reductase inhibitor. We evaluate the frequency of these symptoms in the Prostate Cancer Prevention Trial (PCPT), a large-scale randomized, placebo-controlled trial of finasteride.

METHODS: Records of subjects enrolled in the PCPT were linked to Medicare claims data. Medicare claims were queried for a group of 22 conditions potentially attributed to PFS, including sexual and cognitive symptoms. Logistic regression and Cox regression analyses, comparing former finasteride use to matched placebo, were adjusted for age, race, BMI, and family history of prostate cancer.

RESULTS: Of 18,880 eligible subjects, 15,122 were linked to Medicare; of these 14,239 had one or more years of continuous coverage. Median follow-up from study registration to end of Medicare enrollment was 20 years with 267,983 person-years of follow-up. Of the 22 conditions potentially related to PFS, none had a statistically significant association with treatment arm.

CONCLUSIONS: In the largest placebo-controlled study of the five-alpha reductase inhibitor, finasteride, long-term follow-up does not support the concept of a 'Post-Finasteride Syndrome'. The anecdotal reports to date are likely related to the ubiquitous nature of these symptoms in an aging population and reporting bias.},
}

@article {pmid42628651,
year = {2026},
author = {Slaught, M and Onstad, L and Carpenter, PA and Keel, SB and Lee, CJ and Manjappa, S and Burroughs, L and Mehta, RS and Oshima, MU and Vo, P and Baker, KS and Lee, SJ and Bhatt, NS},
title = {Comparison of Late Effects and Quality of Life by Donor Type in Long-Term Survivors of Severe Aplastic Anemia after Hematopoietic Cell Transplantation.},
journal = {Transplantation and cellular therapy},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.jtct.2026.08.036},
pmid = {42628651},
issn = {2666-6367},
abstract = {BACKGROUND/ OBJECTIVES: With improved outcomes of patients who have undergone allogeneic hematopoietic cell transplantation (HCT) for severe aplastic anemia (SAA), there is a growing population of survivors. Current literature lacks details regarding relevant late effects in these survivors. It is also important to compare late effects and quality of life (QOL) by donor type given the increasing use of alternative donors for HCT in SAA.

STUDY DESIGN: Integral to Fred Hutchinson Cancer Center's long-term follow-up, HCT recipients are sent annual surveys designed to understand patients' health status and QOL. We analyzed surveys of patients who underwent HCT for SAA and responded to a survey between 2015-2023. Self-reported educational/ vocational status, chronic health conditions, medications, and QOL data were captured. QOL was measured using Short-Form 36 (SF-36) questionnaires; scores were normalized to the general population mean of 50 with a standard deviation of 10 points. Multivariable logistic regression was performed to study the associations between donor type and chronic health condition (heart, pulmonary, and renal, musculoskeletal, sexual dysfunction, cataracts) and medication (cardiopulmonary, metabolic/ skeletal, endocrine, gastrointestinal, emotional health) categories. Multivariable linear regression was used to study the associations between donor type and SF-36 domain and summary scores.

RESULTS: The analysis included 122 survivors who underwent HCT between 1972-2021. The median (range) age at HCT and survey were 20.8 (0.8-67.3) and 51.2 (5.6-78.9) years, respectively. Median interval between HCT and survey was 26.0 (1.1-47.1) years. Most respondents underwent matched related donor (MRD) HCT (n=82, 67%), matched unrelated donor (MUD) HCT being next most common (n=24, 20%), followed by alternative donor HCT (n=16, 13%). Among the 86 patients of employment eligible age, 42 (49%) survivors were working full-time and 21 (24%) part-time at the time of the survey. The most common reported chronic health conditions were problems with sexual desire, erection, ejaculation, vaginal dryness, or pain (35%), cataracts (20%), and reduced bone mineral density (20%). The median number of problems requiring medications were 1 (interquartile range 0-3); most used for hypertension (34%), gastroesophageal reflux (22%), and high cholesterol (21%). Compared to survivors after MRD HCT, those after alternative donor HCT (OR 9.9, 95% CI 1.8, 54.1) were more likely to report chronic health conditions affecting the musculoskeletal system. Among 96 respondents who provided SF-36 data, mean (SD) physical component summary score of 49.5 (11.0) and the mental component summary score of 49.9 (12.3) were comparable to general population norms. Compared to MRD, survivors after MUD HCT were noted to have a better score for bodily pain (parameter estimate 9.2, 95% CI 1.4, 17.0). No significant associations between donor types and SF-36 scores were noted in any of the other domains.

CONCLUSIONS: Patients undergoing HCT for SAA remain at risk for late effects emphasizing the need for lifelong monitoring. However, it is encouraging to find that QOL among long-term survivors were similar to that of the general population. We did not detect statistically significant differences in late effects or QOL by donor type, although comparisons were limited by sample size and survivor/respondent bias.},
}

@article {pmid42628810,
year = {2026},
author = {Colbert, C and Komakech, I and Kavuma, A and Kibudde, S and Ford, E and Yorke, A},
title = {Implementation of a radiation oncology incident learning system in a limited resource setting: risk analysis and safety culture.},
journal = {International journal of radiation oncology, biology, physics},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.ijrobp.2026.07.067},
pmid = {42628810},
issn = {1879-355X},
abstract = {PURPOSE: Few reports address the use of incident learning systems (ILS) in low- and middle-income countries (LMICs). We hypothesize that ILS can support quality improvement (QI) needs in an LMIC clinic, and that a commitment to QI can overcome perceived barriers to ILS uptake.

METHODS: A preliminary survey assessing safety culture and perceived barriers to ILS use was distributed to all clinical staff at a radiation oncology clinic in sub-Saharan Africa. An ILS was implemented based on the International Atomic Energy Agency taxonomy. After seven months, ILS reports were analyzed by type, clinic area, clinical role, and origin. Quality control quantification (QCQ) was used to determine the QA intervention most likely to prevent or detect each error. An interdisciplinary team of clinicians used failure modes and effects analysis (FMEA) to rank 23 representative failure modes by risk priority number (RPN).

RESULTS: Survey responses indicated that "concern on the part of the reporter about their reputation or the effects of reporting a colleague" was a barrier to incident reporting. Despite this, the ILS collected eighty-four reports throughout the seven-month accrual period. Most were classified as near-misses (32, 38%). Although most reports were entered from the LINAC control rooms (41, 48.8%), treatment planning was the most common origin of errors (28, 33.3%). The most frequently identified QA intervention that would have prevented errors was a comprehensive physics plan check (29 reports). The highest-RPN failure mode was associated with a treatment delivery error related to the oncology information system (OIS).

CONCLUSION: ILS reports indicate that QI needs center on treatment planning and technical plan review, as well as OIS implementation. This study, one of the few to explore the use of ILS in the LMIC setting, illustrates how a commitment to QI can overcome perceived barriers to ILS use.},
}

@article {pmid42631260,
year = {2026},
author = {Qiu, J and Zhao, YQ and Wei, J and Chinnaiyan, AM and Tosoian, J and Zheng, Y},
title = {Optimizing Sequential Decision Rules for Prostate Cancer Biopsy Management: A Multi-Objective Statistical Framework.},
journal = {Journal of the American Statistical Association},
volume = {},
number = {},
pages = {},
pmid = {42631260},
issn = {0162-1459},
support = {U24 CA288185/CA/NCI NIH HHS/United States ; U2C CA271854/CA/NCI NIH HHS/United States ; U24 CA086368/CA/NCI NIH HHS/United States ; R01 CA236558/CA/NCI NIH HHS/United States ; P50 CA186786/CA/NCI NIH HHS/United States ; },
abstract = {Binary medical decision-making increasingly demands sequential diagnostic strategies that optimize accuracy while minimizing patient burden and healthcare costs. In prostate cancer diagnosis, many patients undergo unnecessary biopsies despite existing biomarkers and imaging tests that already inform risk stratification. Sequential testing, where tests are selectively administered based on prior results, offers a promising approach to balance diagnostic power with procedural efficiency. We propose a novel framework for deriving optimal sequential decision rules using a multi-objective optimization perspective. Specifically, we aim to (1) minimize unnecessary invasive procedures while maintaining sensitivity to underlying disease, and (2) reduce procedural costs by limiting the number of subsequent tests. Rather than collapsing multiple goals into a single weighted score, which forces subjective choices about trade-off weights, we optimize one target while requiring the others to meet prespecified standards. This constrained formulation can be solved efficiently using Lagrange multipliers, yielding a family of optimal sequential rules and a trade-off curve that summarizes the best achievable balance among sensitivity, specificity, and testing burden for clinical protocol design. In the prostate cancer diagnostic data with biomarker and imaging measurements and biopsy-confirmed outcomes, the sequential strategies identify testing pathways that reduce unnecessary procedures while preserving diagnostic quality.},
}

@article {pmid42632449,
year = {2026},
author = {Glascock, M and Wangen, M and Ferrari, RM and O'Leary, MC and Schwartz, J and Ndugulile, M and Unger, JM and Li, L and Marciniak, MW and Reuland, DS and Watabayashi, K and Brenner, AT and Wheeler, SB and Shah, PD},
title = {Expanding access to colorectal cancer screening through community pharmacies: Study protocol for the PharmFIT™ randomized controlled trial.},
journal = {Contemporary clinical trials},
volume = {170},
number = {},
pages = {108443},
doi = {10.1016/j.cct.2026.108443},
pmid = {42632449},
issn = {1559-2030},
abstract = {BACKGROUND: Colorectal cancer (CRC) is a leading cause of cancer death. Fecal immunochemical test (FIT) screening remains underused, particularly in underserved communities. Community pharmacies are highly accessible and increasingly deliver preventive care, yet pharmacy-based CRC screening has not been tested in a large pragmatic randomized trial with concurrent implementation and economic evaluation. This protocol describes a pragmatic trial testing a pharmacy-based CRC screening intervention using FIT, called PharmFIT™, which integrates community pharmacies into CRC screening pathways for primary care patients due for screening.

METHODS: PharmFIT™ is a two-arm, pragmatic, hybrid type 1 effectiveness-implementation trial in two geographically disparate states (Washington and North Carolina). Adults aged 45-75 years, due for CRC screening, are randomized (n = 1200) to PharmFIT™ or usual care. In the intervention arm, clinics recommend CRC screening and refer participants to partner pharmacies, and pharmacists counsel participants, dispense FIT kits, and support kit return and follow-up. The primary outcome is completion of any United States Preventive Services Task Force-recommended CRC screening test within 6 months. Secondary outcomes include reach, timeliness of FIT completion and follow-up colonoscopy, and screening differences across participant subgroups. Implementation outcomes (acceptability, appropriateness, feasibility, fidelity, cost) are assessed using mixed methods, and economic analyses estimate intervention implementation costs, incremental cost per additional participant screened, and budget impact conducted from pharmacy and societal perspectives.

CONCLUSIONS: PharmFIT™ will provide effectiveness, implementation, and cost evidence for pharmacy-based CRC screening, informing the scalability of pharmacist-led cancer prevention within primary care.

TRIAL REGISTRATION: ClinicalTrials.gov (NCT06656936).},
}

@article {pmid42624289,
year = {2026},
author = {Pidala, J and Choe, H and Alousi, A and Kitko, CL and Onstad, L and Mehta, R and Desatnik, G and Wu, QV and Lee, SJ},
title = {Acalabrutinib for treatment of steroid-refractory chronic graft vs. host disease.},
journal = {Transplantation and cellular therapy},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.jtct.2026.08.032},
pmid = {42624289},
issn = {2666-6367},
abstract = {Novel therapies are needed in steroid-refractory chronic graft vs. host disease (SR-cGVHD). We tested acalabrutinib for SR-cGVHD in a multicenter phase II trial (NCT04198922). The primary endpoint was NIH best overall response rate (ORR, comprised of complete (CR) and partial (PR) responses). Secondary endpoints were safety, duration of treatment response, patient-reported outcomes, and failure-free survival (FFS). Included subjects (N=50) were age ≥ 18 with active NIH moderate-severe cGVHD despite prior steroid therapy. Acalabrutinib was given at 100mg orally twice daily for 28 day cycles with intent to complete at least 6 treatment cycles. Responding patients could continue through 24 cycles. Median time from cGVHD diagnosis to enrollment was 31.6 months (IQR 10.1-49.6 months). Participants had received a median of three prior lines of systemic cGVHD therapy including prior ruxolitinib (56%) and belumosudil (48%). Best ORR of all participants was 62% (95% CI 47-75%) by 6 months, and responders showed median duration of response of 28 weeks. Best ORR in those completing at least one cycle of therapy (45 subjects) was 69% (95% CI 53-82%). FFS of the entire population was 59% at 6 months, and 38% at 1 year. Discontinuation of acalabrutinib for toxicity within 6 cycles occurred in 18% of subjects. A total of 27% of subjects demonstrated clinically meaningful improvements in Lee Symptom Scale summary score, and this was not significantly different between responders vs. non-responders. Primary results from this phase II trial demonstrate activity of acalabrutinib in SR-cGVHD.},
}

@article {pmid42627360,
year = {2026},
author = {Okines, AFC and Roesch, E and Watkins, K and Pitner, MK and Hutchinson, KM and Simon, S and Yan, F},
title = {Clinical management of adverse events in patients with advanced HER2+ metastatic breast cancer treated with tucatinib, trastuzumab, and capecitabine.},
journal = {The oncologist},
volume = {},
number = {},
pages = {},
doi = {10.1093/oncolo/oyag330},
pmid = {42627360},
issn = {1549-490X},
abstract = {In the HER2CLIMB study (NCT02614794), tucatinib in combination with trastuzumab and capecitabine (TTC) significantly improved progression-free survival and overall survival compared with the placebo combination with a manageable safety profile in patients with human epidermal growth factor receptor 2-positive (HER2+) metastatic breast cancer (MBC). Based on these findings, the TTC regimen was approved by the US Food and Drug Administration in April 2020 for treatment of patients with HER2+ MBC, including those with brain metastases, after receiving at least 1 prior anti-HER2 therapy in the metastatic setting. Currently, the TTC regimen is the preferred option for third-line treatment in HER2+ MBC and is an option in the second-line setting for patients with brain metastases. As a multidrug regimen, TTC offers enhanced efficacy with dual inhibition of HER2, both extra- and intracellularly, added to the cytotoxic actions of capecitabine. However, some challenges exist with the TTC regimen related to off-target specific drug toxicities and overlapping adverse events (AEs); the most common being diarrhea, liver enzyme elevations, and palmar-plantar erythrodysesthesia. This article aims to describe the clinical presentation of AEs most frequently requiring dose modifications of the TTC regimen and review their clinical management detailed with visual algorithms that incorporate expert medical guidance gained from experience in managing the TTC regimen in routine clinical practice. With the evolving treatment landscape in earlier line settings for HER2+ MBC, patients may now be treated with different first- and second-line therapies from those available when HER2CLIMB was conducted and this may impact its safety profile.},
}

@article {pmid42620287,
year = {2026},
author = {Yu, M and Xie, Y and Allen, L and Carter, K and Donato, E and Cheng, L and Kendziorski, C and Matkowskyj, KA and DeMarzo, AM and Hicks, J and Reddi, D and Newell, EW and Sun, W and Grady, WM},
title = {Spatial multi-omics and single-cell transcriptomics uncover senescence-associated cellular programs during colon adenoma to cancer progression.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
pmid = {42620287},
issn = {2692-8205},
support = {R50 CA233042/CA/NCI NIH HHS/United States ; U01 AG077920/AG/NIA NIH HHS/United States ; U2C CA271902/CA/NCI NIH HHS/United States ; R01 CA264646/CA/NCI NIH HHS/United States ; U54 CA274374/CA/NCI NIH HHS/United States ; },
abstract = {Colorectal cancer develops through a normal-adenoma-carcinoma sequence, yet only 5-10% of adenomas progress to malignancy, and the cellular programs governing that sequence remain poorly defined. Here we generate a spatial multi-omics atlas of human colon adenomas, combining Visium CytAssist and protein co-detection across 24 nonadvanced and advanced tubular adenomas with single-cell resolution Xenium Prime 5K profiling of 101 patient-matched normal, adenoma, and carcinoma cores from 16 patients. Integrating whole-transcriptome and 31-plex protein data identifies nine spatial clusters and two dysplastic epithelial populations that co-express stemness, proliferation, and senescence programs. These programs occupy a shared, spatially confined epithelial niche that expands from adenoma to carcinoma. Spatial analysis revealed GDF15, a senescence-associated secretory factor, mediated the coupling between senescence and stemness in advanced adenomas, and that GDF15-high epithelium locally excludes CD8+ T cells in adenoma and, more broadly, in carcinoma. These findings position senescence as a spatially instructive rather than merely tumor-suppressive program during colorectal carcinogenesis and suggest GDF15 might be a potential candidate target for cancer prevention and interception in the colon.},
}

@article {pmid42622524,
year = {2026},
author = {Schwartz, LF and Gracia, CR and Seshan, VE and Ginsberg, JP and Aplenc, R and Sylvain, G and Friedman, DL and Armenian, SH and Meacham, LR and Chow, EJ and Levine, JM},
title = {Longitudinal Ovarian Reserve in Female Adolescents/Young Adults With Lymphoma: A Report From Children's Oncology Group Study ALTE11C1.},
journal = {Pediatric blood & cancer},
volume = {},
number = {},
pages = {e70641},
doi = {10.1002/1545-5017.70641},
pmid = {42622524},
issn = {1545-5017},
support = {//Leukemia & Lymphoma Society (Translational Research Program)/ ; U10CA180886//National Cancer Institute (NCI)/ ; U10CA098543//National Cancer Institute (NCI)/ ; UG1CA189955//National Cancer Institute (NCI)/ ; U10CA095861//National Cancer Institute (NCI)/ ; 3U10CA180886-10S4//National Cancer Institute (NCI)/ ; L40 CA274778//National Cancer Institute (NCI)/ ; P30CA008748//National Cancer Institute (NCI)/ ; CA240267//United States Department of Defense/ ; //Conquer Cancer, the ASCO Foundation (Career Development Award)/ ; },
abstract = {BACKGROUND: Children's Oncology Group (COG) study ALTE11C1 prospectively evaluated ovarian reserve in female adolescents/young adults (AYAs) with lymphoma from diagnosis to 1 year post-end of treatment (EOT). Healthy peers provided normative comparisons.

PROCEDURE: From 2013 to 2018, female participants ≥6 months post-menarche with newly diagnosed lymphoma were enrolled at COG institutions, along with healthy peers. All completed study entry questionnaires and menstrual cycle-independent blood draws for anti-Müllerian hormone (AMH), follicle-stimulating hormone (FSH), and estradiol; lymphoma participants had four additional draws during and after treatment. Associations between biomarkers, disease and treatment characteristics were evaluated. Logistic regression and recursive partitioning analyses identified predictors of diminished ovarian reserve (DOR: AMH <1 ng/mL) at 1 year post-EOT.

RESULTS: Analyses included 168 participants and 125 healthy peers. Participants had lower AMH than healthy peers at study entry (2.1 vs. 4.1 ng/mL; p < 0.01) and 1 year post-EOT (1.7 vs. 4.1 ng/mL; p < 0.01). AMH declined during treatment, with partial recovery post-EOT to below study entry levels (p < 0.01). Those with advanced stage Hodgkin lymphoma and/or B symptoms had the lowest AMH. By 1 year post-EOT, 34% had DOR; study entry AMH less than 1 ng/mL (p = 0.003) and higher alkylator exposure (p = 0.01) were independent predictors. Most participants with study entry AMH less than 1 ng/mL (76%) or CED ≥6.6 g/m[2] (75%) demonstrated DOR at 1 year post-EOT. No participant had acute ovarian failure at 1 year post-EOT.

CONCLUSIONS: Lymphoma and its treatments affect ovarian reserve in female AYA patients. Low AMH at diagnosis and high alkylator exposure predict post-therapy DOR and can guide fertility preservation counseling.},
}

@article {pmid42623043,
year = {2026},
author = {Ford, E and Stambaugh, C},
title = {Academy of QI-Learning Leadership by Quality Improvement.},
journal = {JAMA oncology},
volume = {},
number = {},
pages = {},
doi = {10.1001/jamaoncol.2026.2940},
pmid = {42623043},
issn = {2374-2445},
}

@article {pmid42623089,
year = {2026},
author = {Unger, JM and Xiao, H and LeBlanc, ML and Hershman, DL},
title = {Federal and Industry Sponsorship in US Cancer Clinical Trials.},
journal = {JAMA oncology},
volume = {},
number = {},
pages = {},
pmid = {42623089},
issn = {2374-2445},
abstract = {IMPORTANCE: Industry and federal sponsors support much of the US cancer clinical trial enterprise. Industry-sponsored trials have traditionally focused on therapeutic development and regulatory approval, whereas federally sponsored trials have been viewed as addressing broader clinical and public health research questions. However, differences between these trial portfolios have not been systematically quantified.

OBJECTIVE: To characterize differences between federally sponsored and industry-sponsored cancer clinical trials in the US.

DESIGN AND SETTING: A comparative study of interventional cancer clinical trial portfolios registered on ClinicalTrials.gov and initiated between 2008 and 2024. US-based interventional cancer trials, including treatment and nontreatment interventions, were included.

EXPOSURE: Lead sponsor classified as federal or industry.

MAIN OUTCOMES AND MEASURES: Trial characteristics, including study purpose, phase, intervention type, deescalation design, rare cancer focus, and patient age category (adult vs children). Differences in trial characteristics by sponsor type were assessed using χ2 tests and described using odds ratios (ORs) with 95% CIs.

RESULTS: Overall, 11 681 federally sponsored trials (n = 2112 [18.1%]) and industry-sponsored trials (n = 9569 [81.9%]) were analyzed. Compared with industry-sponsored trials, federally sponsored trials were less likely to be single-agent drug trials conducted for the purpose of cancer treatment (48.6% vs 77.4%; OR, 0.28; 95% CI, 0.25-0.31; P < .001). In contrast, federally sponsored trials were more likely to evaluate nontreatment interventional trials, including prevention (4.7% vs 1.1%; OR, 4.43; 95% CI, 3.32-5.92; P < .001) and supportive care (2.5% vs 0.9%; OR, 2.92; 95% CI, 2.02-4.20; P < .001). Among trials conducted for the purpose of cancer treatment, federally sponsored studies were more likely to investigate multimodality regimens combining drug and biological agents (19.1% vs 7.4%; OR, 2.98; 95% CI, 2.58-3.44; P < .001) and to combine drug and/or biological agent regimens with radiotherapy (10.5% vs 1.4%; OR, 8.22; 95% CI, 6.51-10.37; P < .001) or surgery (2.5% vs 0.2%; OR, 14.09; 95% CI, 7.95-24.98; P < .001). Federal sponsorship was also associated with greater use of deescalation trial designs (3.1% vs 0.4%; OR, 8.38; 95% CI, 5.43-12.94; P < .001) and trials conducted in rare cancers (17.5% vs 12.1%; OR, 1.54; 95% CI, 1.34-1.77; P < .001) and in children (16.1% vs 5.3%; OR, 3.43; 95% CI, 2.93-4.01; P < .001).

CONCLUSIONS: In this study, industry-sponsored trials were more likely to evaluate single-agent drug therapies, whereas US federally sponsored trials were more likely to evaluate nontreatment interventions, multimodality treatment strategies, treatment deescalation approaches, and therapies for rare cancers and pediatric populations. These findings provide an empirical characterization of the complementary and essential roles of federal and industry sponsors in the cancer clinical trial enterprise.},
}

@article {pmid42623683,
year = {2026},
author = {Anderson, G and Rossouw, J},
title = {Elimination of the Black Box Warning on Menopausal Hormone Therapy.},
journal = {Obstetrics and gynecology},
volume = {148},
number = {3},
pages = {e190},
pmid = {42623683},
issn = {1873-233X},
support = {75N92021D00001, 75N92021D00002, 75N92021D00003, 75N92021D00004, 75N92021D00005./HL/NHLBI NIH HHS/United States ; },
}

@article {pmid42618714,
year = {2026},
author = {Banerjee, R and Hashmi, H and Chaudhary, PM and Atrash, S and Green, K and Ghosh, S and Bixby, T and De Wiest, D and Perciavalle, M and Vesole, DH and Lutfi, F and Jehangir, W and Kaur, G and Khan, AM and Warsame, R and Menon, AP and Price, MA and Murthy, GS and Dima, D and Carney, BJ and Qureshi, ZP and Chhabra, S},
title = {BRIDGE-2M: Optimizing Bridging Therapy Prior to CAR-T Therapy in Multiple Myeloma: A Modified Double-Blind Delphi Panel of US Physicians.},
journal = {Advances in therapy},
volume = {},
number = {},
pages = {},
pmid = {42618714},
issn = {1865-8652},
abstract = {INTRODUCTION: We aimed to achieve consensus on optimal bridging therapy (BT) selection for patients with relapsed/refractory multiple myeloma (RRMM) undergoing chimeric antigen receptor T-cell (CAR-T) therapy.

METHODS: We conducted a double-blind, three-round modified Delphi panel among U.S.-based hematologist-oncologists/hematologists using CAR-T therapy for RRMM.

RESULTS: Panelists (N = 15; all managing -60-100 patients with RRMM within the past year; > 5 years of practice: 86.7%) reached consensus on key attributes influencing BT selection (disease burden, aggressive disease, performance status, comorbidities, line of therapy, age, frailty). Unique patient attributes were linked to clinical objectives (≥ 65 years or frailty: disease stabilization [71% consensus]; poor performance status: end-organ function preservation; comorbidities: functional preservation; high disease burden: preventing clinical decline; aggressive disease: cytoreduction [all 100% consensus]). Goals of BT were to decrease disease burden and promote CAR-T efficacy and safety (100% consensus). While talquetamab was preferred for bridging in later lines (66.7%), 73.3% would consider earlier-line use if approved.

CONCLUSION: This study synthesized expert physician perspectives to develop a consensus-based framework to optimize BT selection, linking five key patient attributes to clinical objectives, with goals extending beyond disease stabilization to enhancing CAR-T efficacy and safety. Graphical abstract available for this article 10.6084/m9.figshare.33016328.},
}

@article {pmid42619260,
year = {2026},
author = {Suger, AH and Harrison, TA and Zhang, J and Wu, MC and Darst, BF and Lindström, S},
title = {The pleiotropic landscape of rare variant associations with multiple cancers in large biobanks.},
journal = {HGG advances},
volume = {},
number = {},
pages = {100662},
doi = {10.1016/j.xhgg.2026.100662},
pmid = {42619260},
issn = {2666-2477},
abstract = {Previous association studies between germline rare genetic variation and cancer risk have primarily examined a limited number of cancers in clinical samples, often with participants predominantly of European genetic ancestry. We conducted exome-wide rare variant association analyses across 70+ cancer types using data from more than 729,000 participants from the UK Biobank (UKB) and All of Us Research Program (AoU) cohorts. We used generalized linear mixed models to screen for cancer pleiotropic effects by conducting gene-based and single variant tests of predicted loss of function (pLoF) and missense variants and six groups of cancer defined by biological and etiological similarities. We then assessed significant genes for associations with 27 individual cancer types that had data for at least 500 cases. Of the 33 potential pleiotropic genes identified, 16 consistently showed significant associations across ≥ 3 individual cancer types. For example, the presence of at least one CHEK2 pLoF variant was associated with increased odds of diagnosis with 14 different cancers (OR range: 1.34 - 3.21). Similarly, the presence of at least one RTEL1 missense variant was associated with lower odds of diagnosis with 9 cancers (OR range: 0.67 - 0.88). Our results expand our knowledge about these loci and point to a larger impact on overall cancer risk than previously appreciated.},
}

@article {pmid42619846,
year = {2026},
author = {Yu, Q and Kim, H and Seidel, S and Acosta-Clark, JF and Martin, BK and O'Connor, K and Daza, RM and Gasperini, M and Nathans, JF and Lam, M and Gamo, E and VijayKumar, S and Kuo, L and Lalanne, JB and Simeonov, K and Pepper, M and Trapnell, C and Gray, JM and Choi, J and Qiu, C and Shendure, J},
title = {In vivo reconstruction of the cell lineage history of a developing mouse with DNA Typewriter, from zygote to late organogenesis.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
pmid = {42619846},
issn = {2692-8205},
support = {P20 GM130454/GM/NIGMS NIH HHS/United States ; P30 CA008748/CA/NCI NIH HHS/United States ; R00 HG012973/HG/NHGRI NIH HHS/United States ; },
abstract = {The complete cell lineage of C. elegans, mapped over four decades ago, was tractable because the animal is small, transparent, and lineage invariant[1]. Most animals are none of these, having orders of magnitude more cells, being opaque, and developing with substantial stochasticity[2]. Since 2016, genome editing-based lineage tracing has opened the door to dense cell lineage reconstruction in such organisms[3-8], but delivering on that promise has proven technically challenging. Here we apply DNA Typewriter[9-11], a prime editing-based recorder that writes stochastic symbolic insertions to an engineered genomic TAPE in strictly sequential order, to trace mouse development from zygote (E0) to late organogenesis (E13.5). We introduce constructs encoding a prime editor, engineered prime editing guide RNAs (epegRNAs), and Pol-III-driven circularized TAPE RNA (circTAPE) into wildtype zygotes by pronuclear injection (PNI), then assay embryos by single-nucleus transcriptional profiling (sci-RNA-seq3)[12] with paired circTAPE recovery. From one E13.5 embryo bearing ~7 integrations of a constitutively expressed prime editor and 11 integrations of 6-unit circTAPE, we recover ~1.75M single-nucleus transcriptomes and reconstruct a time-calibrated phylogeny of 1,340,794 annotated cells with parsimony-based node support. The first cell division is marked unequivocally, and although the resulting blastomeres contribute asymmetrically to the embryo proper, they are fate-neutral and serve as internal replicates that reproduce every finding. A modest cohort of pre-gastrulation founders dominates the embryo, with inequality exceeding neutral expectation within one to two cell cycles of founder allocation, yet these founders remain broadly multipotent; a second phase of clonal dominance arises in specific lineages during organogenesis. At the finest scale, sibling cells share cell type 9-fold in excess of chance, reaching 68- to 107-fold for cell types arising from spatially restricted founder pools, while the recent differentiations of organogenesis are legible in the heterotypic structure of terminal clades. From clade co-occurrence alone, we recover germ-layer organization and a dated hierarchy of cell-type couplings with branch points from E8.5 onwards. Finally, by integrating these data with our single-cell time-series of mouse development[13], we impute transcriptional states and annotations for the majority of internal nodes and recover established state histories for diverse cell types. All data are made freely available, together with NextCell, an interactive browser for this annotated cellular phylogeny of mouse development from zygote to late organogenesis.},
}