@article {pmid41758961,
year = {2026},
author = {Wang, Y and Liu, S and Ghamlouch, H and Gagler, DC and Blaney, P and Nabet, B and Davies, FE and Morgan, GJ},
title = {Study of NSD2 using a dTAG system reveals its molecular mechanism and oncogenic implications in t(4;14) multiple myeloma.},
journal = {Blood},
volume = {147},
number = {24},
pages = {2916-2929},
doi = {10.1182/blood.2025031663},
pmid = {41758961},
issn = {1528-0020},
abstract = {The histone H3 lysine 36 dimethylation (H3K36me2) methyltransferase NSD2 is deleted in Wolf-Hirschhorn syndrome and is aberrantly expressed in 10% to 15% of patients with multiple myeloma (MM) because of a t(4;14) translocation. Although NSD2 is thought to be a primary driver in MM, the exact molecular mechanisms by which it regulates transcription remain unclear. We applied the degradation tag (dTAG) system to acutely degrade NSD2 and used this, in combination with time-resolved thiol-linked alkylation for the metabolic sequencing of RNA (SLAM-seq), to identify 307 transcriptional targets of NSD2. Reconstitution with either wild-type NSD2 or a catalytically inactive mutant (NSD2Y1179A) showed that NSD2's transcriptional effects are almost exclusively dependent on its SET domain activity. Mechanistically, H3K36me2 deposition by NSD2 antagonizes H3K27me3 levels, and treatment with 2 distinct Polycomb repressive complex 2 inhibitors demonstrated that approximately half of the NSD2 target genes are regulated in an H3K27me3-dependent manner. Cleavage under targets and tagmentation (CUT&Tag) analysis showed that upon NSD2 depletion, there was an increase in H3K27me3 that occurred at genome-wide intergenic regions rather than at the promoters or gene bodies of NSD2 target genes. These data suggest that NSD2, via H3K36me2, antagonizes H3K27me3 deposition likely at distal regulatory elements, including enhancers, creating a chromatin landscape favorable for target gene transcription. Importantly, NSD2 target genes were enriched for key oncogenic pathways, and 24 transcription factors (TFs) implicated in neurodevelopment and acute leukemia, consistent with its role in Wolf-Hirschhorn syndrome and MM. Eight of these TFs are known oncogenic drivers in acute leukemia or MM, highlighting a novel molecular mechanism for NSD2's role in t(4;14) MM.},
}

@article {pmid42182279,
year = {2026},
author = {Zhai, Z and Wang, C and Jiang, C and Rong, Z and Li, JJ},
title = {IntegrateRigor: annotation-free integration optimization for cell identity recovery reveals cancer-immune interface niches.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
pmid = {42182279},
issn = {2692-8205},
abstract = {Integrating single-cell and spatial transcriptomics data across batches is essential for recovering comparable cell identities-including cell types, subtypes, and states-as a prerequisite for downstream analyses in multi-condition and large-scale studies. This task remains challenging because between-batch variation removal often conflicts with cell identity preservation, and current methods typically rely on generic highly variable gene selection and lack principled metrics for hyperparameter tuning when cell identity annotations are unavailable. Together, these limitations often lead to over-integration, which merges biologically distinct cell identities, or under-integration, which leaves cells separated by batch rather than identity. Here we introduce IntegrateRigor, a data-driven, annotation-free, method-agnostic framework that optimizes integration specifically for reliable cell identity recovery across batches. IntegrateRigor first selects genes whose expression patterns are stable across batches using a gene-wise likelihood-based batch stability score, excluding batch-sensitive genes that can bias cell identity alignment during integration. It then identifies the optimal integration configuration across methods and hyperparameters by defining a dataset-level integration score that explicitly balances between-batch variation removal against cell identity preservation, without requiring prior annotations. In a colorectal cancer single-cell and spatial transcriptomics dataset, IntegrateRigor revealed previously uncharacterized cancer-immune interface niches in the tumor microenvironment that were masked by under-integration under default settings and by over-integration in previous literature. Across diverse datasets spanning multiple sources of between-batch variation, IntegrateRigor consistently improved cell identity recovery by mitigating both over-integration and under-integration across five state-of-the-art methods. By transforming integration from a heuristic preprocessing step into a statistically principled, dataset-adaptive procedure for cell identity recovery, IntegrateRigor improves the reproducibility and biological discovery power of large-scale single-cell and spatial transcriptomics analyses.},
}

@article {pmid42263665,
year = {2026},
author = {Ueland, K and Elahi, T and Rasmussen, M and Wolfe, AE and Purcell, H and Chakka, SR and Mirimo-Martinez, M and Persinger, H and Johnson, K and Boynton, AM and McMillen, K and Byelykh, M and Biernacki, MA and Yeh, AC and Ali, N and Manjappa, S and Wuliji, N and Fredricks, D and Bleakley, M and Holmberg, LA and Peled, JU and Schenk, J and Raftery, D and Ma, J and Hill, GR and Neuhouser, ML and Lee, SJ and Markey, KA},
title = {Plant-based whole-food diets are feasible during auto-HCT and are associated with dose-dependent microbiome modulation.},
journal = {Blood advances},
volume = {},
number = {},
pages = {},
doi = {10.1182/bloodadvances.2026020270},
pmid = {42263665},
issn = {2473-9537},
abstract = {Plant-based whole foods may represent a tractable approach to mitigating microbiome disruption and improving outcomes in patients undergoing auto-HCT for multiple myeloma, a population in whom intestinal dysbiosis has been linked with inferior survival. We conducted a single-arm clinical trial at our center, in which participants undergoing auto-HCT (n = 22) received fresh, pre-prepared, plant-based meals for 5 weeks spanning conditioning, neutropenia, and early recovery, with the goal of supporting the consumption of nutrient-dense, high-fiber foods. The primary endpoints were feasibility and tolerability, defined by successful enrollment, and patient-reported intake of study meals. Dietary intake was quantified using prospective food diaries and 24‑hour dietary recall surveys. Secondary endpoints included changes in gut microbiome composition and function assessed by shotgun metagenomic sequencing and stool short-chain fatty acid (SCFA) measurements. The intervention was feasible and generally well tolerated, with all participants consuming delivered meals to some degree, with adherence sufficient to support planned dietary and correlative analyses. Greater intake of study meals was associated with more pronounced shifts in gut microbial communities, including enrichment of SCFA-producing taxa and compositional changes consistent with a fiber-responsive microbiome. Stool SCFA concentrations increased from baseline to the end of the intervention, suggesting a functional impact of the dietary strategy on microbial metabolite production during the peri-transplant period. These findings demonstrate that a plant-based meal delivery intervention is implementable during auto-HCT and suggest dose-dependent modulation of the gut microbiome and its metabolic output. The trial is registered at ClinicalTrials.gov (NCT06559709).},
}

@article {pmid42263667,
year = {2026},
author = {Bashey, A and Logan, BR and Hill, LC and Symons, HJ and Farhadfar, N and Grunwald, MR and Pidala, JA and Dehn, JG and Brunstein, C and Arai, S and Leifer, E and He, N and Shaw, BE and Juckett, MB and Devine, SM and Uberti, J and Westervelt, P and Srour, SA and Pusic, I and Vasu, S and Hayes-Lattin, B and Ciurea, SO and Horowitz, MM and Lee, SJ and Hogan, WJ},
title = {Donor-Specific Transplant Outcomes from BMTCTN 1702: A Multi-Center Prospective Biological-Assignment Trial.},
journal = {Blood advances},
volume = {},
number = {},
pages = {},
doi = {10.1182/bloodadvances.2026020355},
pmid = {42263667},
issn = {2473-9537},
abstract = {Newer approaches to control alloreactivity may produce similar transplant outcomes using HLA-mismatched donors versus HLA-matched unrelated donors. However, prospective comparisons are lacking. BMT CTN 1702 used a donor search prognosis score to assign patients without matched sibling donors, to transplant using an 8/8 HLA-matched unrelated donor (MUD) or the center's preference of haploidentical-related (HAPLO), mismatched unrelated (MMUD), or umbilical cord blood (UCB) donors. Outcomes using MUD were compared to HAPLO, MMUD and UCB while adjusting for relevant covariates. Patients (n=1179) (93% adults) underwent transplantation with a MUD (n=772), HAPLO (n=254), MMUD (n=112) and UCB (n=41) at a median of 3.7, 3.4, 3.9 and 3.8 months from enrollment. Post-transplant cyclophosphamide (PTCy) was used in 23.9%, 83.9%, 65.2% and 0% of MUD, HAPLO, MMUD and UCB HCT. In multivariate analysis, compared to MUD, survival after HCT was significantly lower for patients receiving UCB (HR 2.65, p<0.001) but not statistically different for HAPLO and MMUD HCT recipients (HR 1.08 and 1.18). The risk of relapse was not significantly different by donor type, but treatment-related mortality (TRM) (HR 3.31, p<0.001) and disease-free survival (DFS) (HR 1.99, p=0.002) were inferior for UCB but not different for HAPLO and MMUD than MUD. In PTCy patients, HAPLO and MMUD were associated with increased grade 3/4 acute GVHD (HR 2.39, p=0.017 and 2.53, p=0.038) and chronic GVHD (HR 1.71 each, p=0.028 and 0.080) than MUD, but other outcomes were not different. HAPLO or MMUD may effectively be used to expedite transplantation when finding MUD is unlikely. NCT03904134.},
}

@article {pmid42264569,
year = {2026},
author = {Fonseca, GA and Triplette, M},
title = {Lung Cancer Screening Guidelines: Moving Beyond Pack-Years for Equity and Efficiency.},
journal = {Chest},
volume = {169},
number = {6},
pages = {1457-1458},
doi = {10.1016/j.chest.2026.02.029},
pmid = {42264569},
issn = {1931-3543},
}

@article {pmid42265107,
year = {2026},
author = {Agrawal, P and Feng, J and Kallur Siddaramaiah, L and Khechaduri, A and Salladay, KR and Hinton, K and Means, M and Rose, JA and Cohen, L and Tian, M and Baboo, S and Diedrich, JK and Reese, T and Kara, D and Yates, JR and Paulson, JC and Alt, FW and Pancera, M and Stamatatos, L},
title = {Diverse germline-targeting HIV Env immunogens select for distinct mutations in the same knock-in mice B cell receptors.},
journal = {Nature communications},
volume = {},
number = {},
pages = {},
doi = {10.1038/s41467-026-74183-w},
pmid = {42265107},
issn = {2041-1723},
support = {P01 AI138212/AI/NIAID NIH HHS/United States ; R01 AI177095/AI/NIAID NIH HHS/United States ; },
abstract = {VRC01-class HIV broadly neutralizing antibodies have been isolated from people living with HIV. Their unmutated (germline) forms do not bind Env and do not neutralize HIV. They acquire their broadly neutralizing potentials through the accumulation of specific somatic mutations. Here, we identify key modifications that allow Env-derived proteins from diverse HIV clades to effectively engage germline VRC01-class B cell receptors (BCRs) expressed by naive B cells. Noticeably, these germline-targeting Env proteins interact with VRC01-class BCRs differently depending on the specific Env background. When used as immunogens in a knock-in mouse model, all germline-targeting Envs successfully activate VRC01-class B cells. However, the resulting BCRs accumulate distinct mutations at key positions. Thus, while the same BCRs are initially activated, they follow different maturation pathways depending on the immunogen used. These findings have important implications not only for HIV vaccine design efforts but also for other immunogens aiming to direct specific BCR maturation pathways.},
}

@article {pmid42265755,
year = {2026},
author = {Cheng, HH and Maxwell, KN and Salari, K and Cooperberg, MR and Follmer, K and Jeter, JM and Jun, G and Lee, DJ and Patel, HD and Schaeffer, EM and Sokolova, AO and Wolff, EM and Lin, DW},
title = {The 'Prostate Cancer Screening for People at Genetic Risk of Aggressive Disease' (PATROL) study.},
journal = {BJU international},
volume = {},
number = {},
pages = {},
doi = {10.1111/bju.70334},
pmid = {42265755},
issn = {1464-410X},
support = {P50CA097186/NH/NIH HHS/United States ; P50CA180995/NH/NIH HHS/United States ; P50CA272390/NH/NIH HHS/United States ; W81XWH-17-2-0043//DOD Prostate Cancer Research Program/ ; W81XWH-22-2-0021//DOD Prostate Cancer Research Program/ ; HT9425-25-1-0498//DOD Prostate Cancer Research Program/ ; HT9425-25-1-0747//DOD Prostate Cancer Research Program/ ; HT9425-25-1-0544//DOD Prostate Cancer Research Program/ ; //The Canary Foundation/ ; //The Basser Center for BRCA/ ; //BRCA Research and Cure Alliance (CureBRCA)/ ; //The Institute for Prostate Cancer Research/ ; //Polsky Urologic Cancer Institute/ ; //Prostate Cancer Foundation/ ; },
abstract = {BACKGROUND: Inherited (germline) pathogenic and likely pathogenic variants (gPVs) in key genes associated with increased risk of prostate cancer (PCa) now warrant more attentive PCa screening per National Comprehensive Cancer Network (NCCN) guidelines-e.g., BRCA2, HOXB13, ATM, BRCA1, MSH2, MSH6, CHEK2 and TP53. However, the optimal early detection strategy for gPV carriers, including use of age-adjusted PSA thresholds and prostate imaging may be refined. and as a means to investigate novel biomarkers.

STUDY DESIGN: 'Prostate Cancer Screening for People at Genetic Risk of Aggressive Disease' (PATROL) is a multicentre, prospective early detection study for individuals at increased risk for PCa due to carrying a gPV in a PCa risk gene.

ENDPOINTS: The primary endpoint is to determine the positive predictive value of pre-defined age-directed prostate-specific antigen (PSA) level thresholds and prostate-specific imaging, e.g., multiparametric magnetic resonance imaging (MRI) for clinically significant PCa on biopsy for individuals at risk of PCa due to a gPV. Exploratory endpoints include characterising clinicopathological characteristics of PCa and patient-reported outcomes. Biospecimens will be collected to evaluate emerging clinical and research biomarkers.

PATIENTS AND METHODS: Key eligibility includes: individuals aged ≥40 years who carry a gPV in an eligible gene, who have no prior diagnosis of PCa, do not have another active malignancy, and provide informed consent. Study procedures include annual physical examination and PSA. Imaging with MRI is optional at baseline and recommended if the PSA level is above the protocol-recommended PSA level threshold. Participants will be offered prostate biopsy for any clinical concern, PSA level >1.0 ng/mL if aged <50 years; PSA level >1.5 ng/mL if aged 50-59 years; PSA level >2.0 ng/mL if aged ≥60 years. If PCa is diagnosed, clinical care is determined by the participant and treating physician. If opting for active surveillance, study procedures will be collected annually for 10 years or until definitive treatment. If definitive treatment, study procedures will be collected for an additional 1 year. Long-term clinical outcomes will be collected annually until the study closes.},
}

@article {pmid42266673,
year = {2026},
author = {Kirtane, K and Niu, J and Blumenschein, G and Massarelli, E and Hanna, GJ and Lee, S and Bishop, MR and Konecny, GE and Mao, D and Zheng, Y and Rodriguez, K and Kim, JJ and Williams, C and Schweitzer, C and Adhikary, S and Jung, AS and Klebanoff, CA},
title = {A phase 1 trial of HPV16 E7 T-cell receptor-engineered T cells in patients with relapsed/refractory HPV16-positive cancers (KITE-439 trial).},
journal = {Frontiers in oncology},
volume = {16},
number = {},
pages = {1809354},
pmid = {42266673},
issn = {2234-943X},
abstract = {Patients with relapsed/refractory (r/r) HPV-associated epithelial cancers have a poor prognosis. Engineered T cells expressing a T cell receptor (TCR) specific for HPV16 E7 can induce tumor regression. We conducted a Phase 1 trial of KITE-439, an investigational autologous T-cell product expressing TCR specific for HPV16 E7 in patients with r/r HPV16+ epithelial cancers. CD4+ and CD8+ T cells selected from leukapheresed peripheral blood mononuclear cells were stimulated with anti-CD3/anti-CD28 antibodies followed by retroviral transduction and expansion in the presence of interleukin-7/15 and an AKT inhibitor. Patients received lymphodepleting chemotherapy (cyclophosphamide 30 mg/kg/day for 2 days and fludarabine 25 mg/m[2]/day for 5 days) followed by a single infusion of KITE-439 with daily IL-2 (2.5×10[5] IU/kg, up to 7 doses). The primary objectives were safety, tolerability, and efficacy; the primary endpoint was dose-limiting toxicities (DLTs). Eight HLA-A*02:01+ patients received KITE-439 (1×10[6]-1×10[8] cells/kg). No DLTs occurred during the trial. In all patients, KITE-439 cells were detected in peripheral blood within 7 days post-infusion. Three patients experienced Grade 1-2 cytokine release syndrome related to KITE-439 (resolved within 1-5 days) and 4 had KITE-439-related Grade 1-2 neurologic events (resolved within a day). One patient achieved a partial response (from Day 35 to Month 3) and 7 had a best response of stable disease. These results suggest that KITE-439 has an acceptable safety profile for the treatment of patients with HPV-associated epithelial cancers. Further studies are needed to determine optimal manufacturing conditions and T-cell characteristics required for enhanced antitumor activity.},
}

@article {pmid42268934,
year = {2026},
author = {Guzmán-Solís, AA and Ouizougun-Oubari, M and Escaffre, O and Larsen, BB and Lopez, M and Locklear, S and Kumar, M and Juelich, TL and Smith, JK and Zhang, L and Haas, GD and Roenicke, R and Brambilla, L and Oguntuyo, KY and Patel, AR and Sapse, IA and Bowden, TA and Tortorella, D and Bloom, JD and Freiberg, AN and Bajic, G and Duty, JA and Lee, B},
title = {A cocktail of human mAbs targeting the henipavirus fusion and receptor binding proteins provides cross-species neutralization.},
journal = {Science translational medicine},
volume = {18},
number = {853},
pages = {eadw8573},
doi = {10.1126/scitranslmed.adw8573},
pmid = {42268934},
issn = {1946-6242},
mesh = {Humans ; Animals ; *Antibodies, Monoclonal/immunology ; *Henipavirus/immunology ; *Viral Fusion Proteins/immunology ; *Antibodies, Neutralizing/immunology ; Mice ; Neutralization Tests ; Mice, Transgenic ; Cross Reactions/immunology ; *Receptors, Virus/metabolism ; Amino Acid Sequence ; },
abstract = {The Nipah and Hendra viruses (NiV and HeV, respectively) are highly pathogenic, with case fatality rates of 40 to 75%, representing substantial public health threats. Although one monoclonal antibody (mAb), mAb102.4, has advanced through phase 1 clinical trials, there remains a critical need for approved therapeutic options against these henipaviruses (HNVs). Development of human mAbs has been constrained by limited access to convalescent patient samples. Here, we describe human mAbs derived from transgenic humanized mice that cross-neutralize extant NiV and HeV strains by binding to their fusion protein (F) or receptor binding protein (RBP). Deep mutational scanning and functional studies demonstrated that the anti-RBP mAb (8G3) targets the receptor binding site and requires multiple simultaneous mutations for escape. Sequence analysis of our anti-F mAbs identified a clonally expanded VH3-33 family with evidence of somatic hypermutation, yielding high-affinity antibodies. Cryo-electron microscopy revealed that our most potent F antibody (2A1) recognizes a conserved quaternary epitope spanning two protomers in trimeric prefusion NiV-F and stabilized, rather than displaced, a key glycan shield, distinguishing it from previously described antibodies targeting this region. The 8G3 and 2A1 mAbs exhibited additive neutralization when combined and provided complete protection against lethal NiV challenge in hamsters when administered individually or as a cocktail, even when treatment was delayed. Using a pseudovirus system, we show that this dual-targeting approach was resilient against a suite of escape mutants compared with monotherapy. Our findings establish a candidate therapeutic strategy that minimizes development of resistance, providing a foundation for next-generation countermeasures against emerging HNVs.},
}

Humans
Animals
*Antibodies, Monoclonal/immunology
*Henipavirus/immunology
*Viral Fusion Proteins/immunology
*Antibodies, Neutralizing/immunology
Mice
Neutralization Tests
Mice, Transgenic
Cross Reactions/immunology
*Receptors, Virus/metabolism
Amino Acid Sequence

@article {pmid42268936,
year = {2026},
author = {Malek, R and Matassoli, F and Gordon, K and Shimberg, GD and Mantus, GE and Spangler, A and Chopde, AJ and Teng, IT and Zhou, T and Lin, BC and Carroll, R and Kazmierski, R and Wang, L and Posavad, CM and Rouphael, NG and Branche, AR and Roberts, PC and Serebryannyy, L and Andrews, SF},
title = {SARS-CoV-2 variant booster vaccination and infection alter the breadth of the memory B cell repertoire.},
journal = {Science translational medicine},
volume = {18},
number = {853},
pages = {eaeb9847},
doi = {10.1126/scitranslmed.aeb9847},
pmid = {42268936},
issn = {1946-6242},
abstract = {Evolving endemic viruses such as influenza and severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) remain major health threats. Although variant updated vaccines aim to enhance protection, preexisting immunity shapes memory B cell (MBC) responses. To assess how SARS-CoV-2 spike protein variant-based vaccine boosters and infections alter the MBC repertoire, we analyzed MBC responses in the COVAIL vaccine trial, where participants previously vaccinated with SARS-CoV-2 Wuhan-1 spike immunogen were boosted with Wuhan-1, variant, or bivalent spike immunogens. Some participants also experienced a subsequent infection with an Omicron variant. We determined that variant vaccine boosters and SARS-CoV-2 infections led to transiently greater recall of cross-reactive MBCs compared with a Wuhan-1 vaccine booster. Long term, we detected little change in the MBC repertoire after an Omicron vaccine booster, but MBCs evaluated several months after Omicron variant infection had higher neutralization capacity to both Wuhan-1 and BA.1 compared with those from individuals who had not experienced an infection. However, these Wuhan-1/BA.1 cross-reactive MBCs from infected individuals displayed less breadth toward the more distant BA.2.86 lineage than MBCs from uninfected individuals. Thus, SARS-CoV-2 variant boosters and infections differentially shape the long-term MBC repertoire.},
}

@article {pmid42269282,
year = {2026},
author = {Gazeau, S and Byrne, C and Coombs, D and Kunzweiler, C and Calheiros, RC and Diaz-Decaro, J and Gantt, S and Craig, M},
title = {Mathematical modelling highlights the crucial role of early childhood immunization in preventing congenital CMV in countries with high CMV seroprevalence.},
journal = {Vaccine},
volume = {88},
number = {},
pages = {128788},
doi = {10.1016/j.vaccine.2026.128788},
pmid = {42269282},
issn = {1873-2518},
abstract = {BACKGROUND: Congenital cytomegalovirus infection (cCMVi) is a major global health problem and a leading cause of childhood hearing, visual, and intellectual disability. Development of an effective vaccine against CMV is a high priority, and there is optimism that one will be achieved soon. Previous mathematical modelling to predict the impact of CMV vaccination in low CMV seroprevalence, high-income populations indicate that vaccinating infants could be a highly efficient strategy to prevent cCMVi, even with only a modestly effective vaccine (i.e., <50% protective against primary infection). However, whether vaccinating infants is optimal in high CMV seroprevalence settings, where rates of cCMVi are correspondingly higher, is unclear.

METHODS: We adjusted our existing agent-based stochastic model to study CMV vaccine efficacy in high seroprevalence settings (reaching 90%) with Brazil as a test case.

RESULTS: Our results suggest that vaccinating 12-year-old girls and women of childbearing age would have limited ability to reduce cCMVi rates in Brazil, even with a vaccine conferring complete life-long protection against CMV infection. In contrast, vaccinating infants was predicted to provide substantial long-term reductions in the number of cCMVi cases in Brazil, even if it only induced protection equivalent to natural immunity against CMV reinfection and reactivation. Further, our model predicted that if two-thirds of Brazilian infants were vaccinated, a modestly effective vaccine would reduce the number of cCMVi cases by up to 76%.

CONCLUSION: Together with results from other studies, this analysis underscores that infancy is likely the optimal target age for CMV vaccination to prevent cCMVi in all populations, regardless of the CMV seroprevalence. Furthermore, our findings predict large reductions in disease due to cCMVi worldwide through attainable vaccination scenarios.},
}

@article {pmid42270451,
year = {2026},
author = {Schwartz, J and Meehan, K and Cohn, EB and Bacci, JL and Calo, WA and Ko, LK and Shah, PD},
title = {Current practices, opportunities to improve, and behavioral targets related to HPV vaccination in community pharmacies: A qualitative study of pharmacy staff and parents.},
journal = {Human vaccines & immunotherapeutics},
volume = {22},
number = {1},
pages = {2685449},
doi = {10.1080/21645515.2026.2685449},
pmid = {42270451},
issn = {2164-554X},
abstract = {Human papillomavirus (HPV) causes 39,300 cancers annually in the United States, yet adolescent vaccination coverage remains suboptimal. Community pharmacies are highly accessible and authorized to vaccinate adolescents but remain underutilized for HPV vaccination. This study examined how current pharmacy vaccination practices align with parent expectations and identified modifiable behavioral and implementation targets to improve uptake. We conducted a qualitative study using key informant interviews with pharmacy staff (n = 11) and parents of adolescents ages 9-17 (n = 13) between February - March 2021. Interview guides were informed by the 5As Behavioral Counseling Framework and Theoretical Domains Framework (TDF). Data were analyzed using framework-guided rapid content analysis to identify themes related the vaccination workflow stages. Analyses identified 31 current practices and 35 opportunities for improvement across the 5As, as well as 20 behavioral constructs spanning 12 domains. Key gaps identified by pharmacy staff included inconsistent adolescent vaccine assessment, limited proactive recommendations, lack of standardized communication, insufficient documentation and follow-up for hesitancy, and fragmented reminder and scheduling systems. Parents valued convenience and clear, concise recommendations, while staff highlighted workflow and system constraints. Opportunities centered on standardizing assessment and communication, expanding technician roles, implementing proactive prompts and reminders, improving care coordination with primary care providers, and strengthening follow-up processes. Pharmacy-based HPV vaccination can be strengthened through targeted behavioral and workflow changes across the vaccination continuum. These findings provide a theory-informed, practice-ready framework to guide intervention design and evaluation aimed at increasing HPV vaccine uptake and series completion in community pharmacy settings.},
}

@article {pmid42273705,
year = {2026},
author = {Monaco, F and Tran, DT and Sandmaier, BM and Tykodi, SS},
title = {Case Report: donor cell-derived leukemia after allogeneic stem cell transplantation for metastatic renal cell carcinoma.},
journal = {Frontiers in immunology},
volume = {17},
number = {},
pages = {1830323},
pmid = {42273705},
issn = {1664-3224},
abstract = {Donor cell-derived leukemia (DCL) is a rare complication of allogeneic hematopoietic cell transplantation (allo-HCT), previously described in patients receiving allo-HCT for hematologic malignancies. Allo-HCT has also been investigated as an immunotherapy platform for solid tumors including clear cell renal cell carcinoma (RCC). Herein, we describe a unique patient case treated by allo-HCT for RCC who subsequently developed DCL. A 40-year-old man was diagnosed with metastatic clear cell RCC treated surgically by left nephrectomy plus metastasectomy of a rib lesion. He was referred to the Fred Hutchinson Cancer Center and treated by allo-HCT as part of a clinical trial (NCT00005851). His initial allograft following fludarabine/2 Gy total body irradiation (TBI) conditioning was complicated by graft failure. After collecting a G-CSF-mobilized autologous hematopoietic stem cell product as a failsafe for repeated graft failure, he was re-transplanted from the same donor following cyclophosphamide/antithymocyte globulin (ATG) conditioning, resulting in successful engraftment. Fourteen months later, he developed donor origin acute myelomonocytic leukemia with central nervous system (CNS) involvement. He was treated by 7 + 3 induction with intrathecal methotrexate and was able to achieve complete remission. He subsequently underwent autologous hematopoietic cell transplantation (auto-HCT) without further leukemia relapse. Unfortunately, 4 years after his auto-HCT, he developed recurrent RCC, initially managed by surgical resections. Upon further progression, he was then treated with sequential lines of systemic therapy that included pazopanib, nivolumab, cabozantinib, and lenvatinib/everolimus. He died from complications of his RCC 17 years after his second successful allograft. The absence of pre-transplant systemic therapies for the patient's metastatic RCC and ongoing good health of the donor implicates a leukemogenic potential of his transplant-associated therapies including TBI, cyclophosphamide, and ATG. His uncommonly long survival from metastatic RCC suggests clinical benefit was derived from the 14-month duration of allo-HCT associated with T-cell allo-immunity previously shown capable of targeting RCC-associated minor histocompatibility antigens.},
}

@article {pmid42124731,
year = {2026},
author = {Harari, S and Eguia, RT and Dadonaite, B and Radford, CE and Stewart, C and Veesler, D and Bloom, JD},
title = {Mutations to the HCoV-229E spike have counterbalancing effects on serum antibody neutralization and receptor binding.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
pmid = {42124731},
issn = {2692-8205},
abstract = {Human coronavirus 229E (HCoV-229E) is an endemic pathogen that causes repeated "common-cold" infections throughout life. Like other coronaviruses, it accumulates spike mutations that erode antibody immunity and enable reinfection. Here, we use pseudovirus deep mutational scanning to measure how mutations to the HCoV-229E spike affect its cell entry function, binding to its human APN receptor, and neutralization by human sera with a range of sensitivities to erosion by viral evolution. We find that both receptor binding and serum neutralization are affected by mutations across spike, including many that modulate these properties by affecting the balance of up versus down conformations of the spike receptor-binding domain (RBD). In particular, some mutations increase both receptor binding and serum neutralization by shifting the RBD to a more up conformation, suggesting that the HCoV-229E spike has evolved to shield key RBD neutralizing epitopes at the cost of less efficient receptor binding.},
}

@article {pmid42256204,
year = {2026},
author = {Yang, Y and Ronsley, R and Kilburn, L and Kim, A and Wechsler-Reya, RJ and Yang, ZJ},
title = {Differentiation-inducing triiodothyronine enhances chemotherapy and suppresses post-treatment tumor regrowth in medulloblastoma.},
journal = {Molecular therapy. Oncology},
volume = {34},
number = {2},
pages = {201235},
pmid = {42256204},
issn = {2950-3299},
abstract = {Medulloblastoma (MB), the most common malignant pediatric brain tumor, is treated with intensive multimodal regimens that cause substantial long-term toxicity and fail to prevent recurrence in up to 30% of patients. We investigated triiodothyronine (T3), an FDA-approved thyroid hormone, as a differentiation-based therapeutic strategy for MB. Using a Sonic Hedgehog (SHH)-driven mouse model, two patient-derived xenografts (SHH and group 3), and drug-resistant TP53-mutant MB cells, we found that T3 and cytotoxic chemotherapy suppress tumor growth through complementary biological mechanisms: T3 promotes terminal differentiation of tumor cells, whereas cyclophosphamide (CTX) and irinotecan (CPT-11) induce caspase-3-dependent apoptosis. In vitro, T3 enhanced the tumor inhibitory effects of CTX and CPT-11, suppressed proliferation in chemotherapy-resistant cells, and promoted differentiation across MB subgroups. In vivo, sequential administration of T3 following chemotherapy suppressed post-treatment tumor regrowth and prolonged survival without increasing systemic toxicity. T3-induced transient tachycardia was effectively controlled with propranolol without compromising antitumor activity. Together, these findings support the potential of T3 as a clinically accessible differentiation-based therapy that enhances chemotherapy responses and suppresses post-treatment tumor regrowth in medulloblastoma.},
}

@article {pmid42256618,
year = {2026},
author = {Zane, GK and Dimitrov, D and Levin, CE and Khosropour, CM and Duerr, A},
title = {Evaluating the potential health and economic impacts of chlamydia vaccination strategies in the United States: a mathematical modeling and cost-effectiveness simulation study.},
journal = {Lancet regional health. Americas},
volume = {60},
number = {},
pages = {101502},
pmid = {42256618},
issn = {2667-193X},
abstract = {BACKGROUND: Chlamydia trachomatis (chlamydia) is the most commonly reported sexually transmitted infection in the United States (US), causing substantial morbidity and costs despite effective treatment. Vaccination may be a promising prevention strategy, but its national epidemiologic and economic impact remains understudied.

METHODS: We developed an age- and sex-structured compartmental model of heterosexual chlamydia transmission among US individuals aged 15-64 years from 2000 to 2075. The model was calibrated to adjusted annual chlamydia cases and validated against national prevalence data. We simulated routine vaccination of adolescent females or both sexes beginning in 2025, with or without a one-time catch-up campaign for unvaccinated females aged 15-24 years in 2035. Outcomes included chlamydia incidence rates, infections and sequelae averted by 2075, and incremental cost-effectiveness ratios through 2050.

FINDINGS: Without vaccination, incidence rates were projected to rise from 16.9 to 18.7 infections per 1000 person-years between 2025 and 2075. Under base-case assumptions (50% coverage, 70% efficacy, 10-year protection), incidence rates declined to 4.0 and 0.4 per 1000 person-years under female-only and sex-neutral vaccination, respectively. By 2075, female-only and sex-neutral vaccination reduced infections by 37.4% and 52.3%, respectively. Catch-up vaccination provided modest additional benefit. All strategies were cost-saving; sex-neutral vaccination yielded 145,943 additional quality-adjusted life years and $354 million in savings versus female-only vaccination by 2050. Results were robust across sensitivity analyses.

INTERPRETATION: Chlamydia vaccination could substantially reduce infections and sequelae in the US and is likely to be cost-saving or highly cost-effective across plausible scenarios.

FUNDING: This work was primarily supported by the National Institutes of Health (1F31AI181431-01A1).},
}

@article {pmid42258320,
year = {2026},
author = {Kleeman, SO and Riazat-Kesh, Y and Carvajal, R and Marmarelis, ME and Schadendorf, D and Sharon, E and Othus, M and Robert, C and Skoulidis, F and Izar, B and Maki, RG and Janowitz, T},
title = {Cancer chemo-immunotherapy: time will tell.},
journal = {Cancer immunology research},
volume = {},
number = {},
pages = {},
doi = {10.1158/2326-6066.CIR-26-0335},
pmid = {42258320},
issn = {2326-6074},
abstract = {Endogenous circadian programs coordinate physiology across tissues, including immune cell trafficking and drug metabolism. Previous retrospective studies suggested that the timing of immune checkpoint inhibitor delivery may be a modifiable determinant of survival in patients with cancer, with earlier infusions often associated with improved outcomes. Recently, the prospective randomized phase 3 LungTIME-C01 trial reported that earlier time-of-day (before 3pm) administration of chemo-immunotherapy nearly doubled progression-free survival in patients with non-small cell lung cancer. In this commentary, we examine the trial's clinical design and execution, including protocol amendments and safety reporting that warrant clarification. We consider the mechanistic interpretation of the results, highlighting that the observed effects may reflect contributions from cytotoxic chronopharmacology, circadian immune regulation, and healthcare delivery factors rather than immunotherapy timing alone. We outline implications for future trial design, including factorial approaches to disentangle the timing of immunotherapy from chemotherapy and the need for multicenter validation before scheduling recommendations are widely adopted.},
}

@article {pmid42258780,
year = {2026},
author = {Unger, JM},
title = {Psychosocial Predictors of Shared Decision Making Among US Cancer Survivors.},
journal = {JCO oncology practice},
volume = {},
number = {},
pages = {OP2501143},
doi = {10.1200/OP-25-01143},
pmid = {42258780},
issn = {2688-1535},
abstract = {PURPOSE: Cancer survivors, who have unique health care needs, are projected to number nearly 19 million by 2025, over 5% of the US population. Shared decision making (SDM) between patients and providers is vital for patient-centered care. This study evaluated whether demographic, socioeconomic, behavioral, geographic, health, health information, and psychosocial factors predict the risk of cancer survivors not engaging in SDM.

METHODS: Data from the Health Information National Trends Survey (HINTS) from 2012 to 2024 were used. Participants included adults diagnosed with cancer within the past 20 years who had one or more health care visits in the past year. SDM was measured on a four-point scale by a question about involvement in health care decisions, with dichotomization (always v usually/sometimes/never) aligned with Healthy People 2030 objectives. Forty-two variables were analyzed, and a risk prediction model was developed using 60% of the participants and validated with the remaining 40%.

RESULTS: The study included 3,622 participants, predominantly older than 65 years (61.5%), with 54.8% being women and 12.9% Black. A model with four variables (distrust of health care providers, distrust of family, anxiety/depression, and fair/poor perceived health) was associated with lower SDM engagement in the training set and was confirmed in the validation set. For each increase in the quartile level of adverse risks, there was a 23% reduction in the odds of SDM. The odds of experiencing SDM were 56% lower for those with 3-4 risk factors than for those with 0 risk factors.

CONCLUSION: These findings suggest that screening for psychosocial vulnerability may help identify cancer survivors who could benefit from targeted strategies to support SDM in clinical care.},
}

@article {pmid42260942,
year = {2026},
author = {Fathima, S and Wong, MM and Gonzalez-Lugo, J and Geyer, SM and Alsugair, A and Sirenko, M and Langer, KJ and Lasho, TL and Finke, C and Choi, J and Abdul-Hay, M and Ho, G and Litzow, MR and Matin, A and Durani, U and Hefazi, M and Hogan, WJ and Shah, MV and Al-Kali, A and Begna, KH and Gangat, N and Saliba, AN and Go, RS and Kewan, T and Bartoo, G and Kutzke, J and McCullough, K and Warrington, KJ and Sullivan, M and Reichard, KK and Olteanu, H and Murthy, H and Badar, T and Kusne, Y and Palmer, J and Chhabra, S and Punwani, N and Riwes, M and McGuirk, JP and Krakow, EF and Langston, A and Kourelis, T and Dingli, D and Foran, J and Koster, MJ and Patnaik, MM and Beck, DB and Alkhateeb, HB and Mangaonkar, AA},
title = {Therapeutic Outcomes in VEXAS Syndrome: A Multicenter Comparative Cohort of Allogeneic Hematopoietic Stem Cell Transplantation and Hypomethylating Agents.},
journal = {American journal of hematology},
volume = {},
number = {},
pages = {},
doi = {10.1002/ajh.70401},
pmid = {42260942},
issn = {1096-8652},
support = {Arnold and Kit Palmer Career Award in Cancer Research//Mayo Clinic Center for Clinical and Translational Science/ ; CSDG-23-1020347-01-IBCD//American Cancer Society/ ; },
abstract = {Hypomethylating agents (HMA) and allogeneic hematopoietic stem cell transplantation (alloHSCT) have both demonstrated remissions in VEXAS; however, comparative data is lacking. We conducted a multicenter, retrospective analysis of 66 patients diagnosed with VEXAS syndrome treated with HMA (n = 35) or alloHSCT (n = 31). Baseline characteristics such as genetics, co-morbidities, and performance status were balanced between the groups, except older age in the HMA group. Median follow-up from therapy initiation was 18 months (95% CI: 11-26), and 14 (21%) deaths were reported (alloHSCT n = 3; HMA n = 11). Among all evaluable patients within the alloHSCT cohort, all patients achieved molecular remission, and a substantial proportion of patients discontinued glucocorticoids (58%). In contrast, HMA therapy was associated with lower but meaningful rates of molecular remission (22%) and glucocorticoid discontinuation (6%). In a real-world setting, HMA therapy was associated with a high discontinuation rate related to toxicity or lack of response. On multivariable analysis adjusted for age and Charlson Comorbidity Index, alloHSCT was associated with improved overall survival (HR = 0.20, 95% CI: 0.05-0.81; p = 0.024). This association remained consistent across multiple ancillary sensitivity analyses, including restriction to transplant-eligible patients, patients aged ≤ 75 years, 1:1 matching, and propensity score-based weighted analyses. Although limited by retrospective design, these findings suggest that alloHSCT remains an attractive and potentially curative strategy in selected patients with VEXAS. Prospective validation of these findings is warranted.},
}

@article {pmid42262514,
year = {2026},
author = {Chlebowski, RT and Rapp, S and Aragaki, AK and Manson, JE and Pan, K and Neuhouser, ML and Johnson, KC and Snetselaar, LG and Henderson, VW and Qi, L and Hayden, KM and Baker, LD and Garcia, O and Pichardo, MD and Wactawski-Wende, J and Prentice, RL},
title = {Low-fat dietary pattern and dementia mortality: a secondary analysis of the Women's Health Initiative dietary modification randomized clinical trial with long-term follow-up.},
journal = {Menopause (New York, N.Y.)},
volume = {},
number = {},
pages = {},
pmid = {42262514},
issn = {1530-0374},
abstract = {OBJECTIVES: In the Women's Health Initiative (WHI) Dietary Modification (DM) randomized trial, the dietary intervention significantly reduced breast cancer mortality and, in a subgroup of women 65 years old or above, significantly lowered possible cognitive impairment based on Modified Mini-State Examination (3MSE) scores. Based on this background, we examined the dietary intervention association with long-term dementia mortality.

METHODS: The WHI DM clinical trial randomized 48,835 postmenopausal US women, aged 50-79 years, with dietary fat intake ≥32% of energy and anticipated ≥3-year survival. Cognitive function was not an eligibility criterion. Randomization was to a low-fat dietary pattern intervention (40%; n=19,541) with goals to reduce fat intake and increase fruit, vegetable, and grain intake or a usual diet comparison (60%; n=29,294). All dietary targets were significantly reduced. Mortality findings were confirmed by central medical record review enhanced by serial National Death Index findings. Dementia mortality was examined after an 8.5-year (median) dietary intervention and 20-year cumulative follow-up.

RESULTS: Dietary intervention did not influence dementia mortality (n=1,386) (HR: 0.94, 95% CI: 0.85-1.05), with similar findings for Alzheimer (HR: 1.00, 95% CI 0.85-1.17) and non-Alzheimer dementia mortality (HR: 0.90, 95% CI 0.77-1.05). Of 13 subgroup analyses, with dietary intervention, there was a trend for lower dementia mortality in younger women (50-59 y, HR: 0.73, 95% CI: 0.44-1.21; 60-69 y, HR: 0.85, 95% CI: 0.72-1.01; 70-79 y, HR: 1.06, 95% CI: 0.91-1.23; P-trend 0.03).

CONCLUSIONS: A low-fat eating pattern did not reduce dementia mortality in postmenopausal women.},
}

@article {pmid42262918,
year = {2026},
author = {Topalidou, I},
title = {A second life.},
journal = {Genetics},
volume = {},
number = {},
pages = {},
doi = {10.1093/genetics/iyag116},
pmid = {42262918},
issn = {1943-2631},
abstract = {The Genetics Society of America Mentorship Award recognizes members of the scientific community for exceptional mentoring of geneticists at any career stage. Irini Topalidou is the inaugural recipient in the nonfaculty category, honored for her outstanding contributions to mentoring within the C. elegans community and beyond. She has mentored numerous trainees who have gone on to pursue graduate and medical degrees, postdoctoral or faculty positions, and careers in biotech. The award further acknowledges her published work on STEM education and career choice, as well as her commitment to understanding and addressing trainee challenges and to improving mentorship practices. In the essay below, Irini reflects on her journey as an immigrant in the United States and how these experiences have shaped her life, career, and approach to mentorship. She also highlights how recent scientific and cultural shifts are challenging the principles of openness, diversity, and discovery in the United States, placing one of its greatest strengths at risk.},
}

@article {pmid42250885,
year = {2026},
author = {Naumova, AV and Nakamura, K and Marchiano, S and Neidig, LE and Blakely, LP and Tsuchida, H and Murry, CE and Kerwin, WS},
title = {Circumferential Strain Recovery After Human Cardiomyocyte Transplantation in Minipigs Using a Novel Frequency-Based Method for Myocardial Tagging Quantification.},
journal = {Journal of cardiovascular magnetic resonance : official journal of the Society for Cardiovascular Magnetic Resonance},
volume = {},
number = {},
pages = {102756},
doi = {10.1016/j.jocmr.2026.102756},
pmid = {42250885},
issn = {1532-429X},
abstract = {BACKGROUND: Transplantation of human pluripotent stem cell-derived cardiomyocytes (hPSC-CMs) is promising new method for heart remuscularization after infarction. We hypothesized that hPSC-CMs affect heart function by improving local contractility in the infarcted zones. However, there is a need for a precise non-invasive assessment of regional contractile function in the infarcted segments.

METHODS: We describe here a novel approach for rapid and robust quantification of myocardial end-systolic circumferential strain (CS). Linear tags are placed in 60-degree pattern offsets and analyzed via optimized post-processing based on local Fourier transformation of standardized American Heart Association (AHA) myocardial segmentation. This method has been implemented for the first time to evaluate transendocardial hPSC-CMs transplantation in a minipig model of myocardial infarction. Validation of the new frequency-based calculation of myocardial strain was done using two independent approaches: (1) a tag tracking, and (2) feature tracking technique.

RESULTS: In the cell-treated hearts (n=4), mean end-systolic CS in the infarcted segments (anterior and anteroseptal areas combined) at the mid-wall region decreased from -6.69 ± 1.56% (pre-MI) to -1.13 ± 1.96% at 2 weeks post-MI (pre-treatment), with subsequent improvement to -4.00 ± 0.76% by 8 weeks after cell transplantation. Conversely, CS in the infarcted segments in vehicle-control group (n=5) decreased from -5.18 ± 0.97% (pre-MI) to -1.39 ± 1.23% at 2 weeks post-MI and worsened further to 0.33 ± 1.93% by 8 weeks post-vehicle. There was no improvement in the global ejection fraction in the cell-treated group in comparison with control. It was a high correlation of the new method of myocardial strain calculation with the standard tag tracking approach and feature tracking strain analysis across the experimental conditions (normal heart, infarcted, cell/vehicle treated).

CONCLUSIONS: A novel frequency-based technique for assessment of local circumferential strain does not require specialized acquisition protocols, access to k-space data, nor highly optimized reconstruction algorithms or commercial software. It can quickly and precisely assess regional myocardial injury and recovery. Our findings support our hypothesis that transplantation of hPSC-CMs improves regional myocardial strain in infarcted minipig hearts.},
}

@article {pmid42252893,
year = {2026},
author = {Mahla, RS},
title = {Identifying Antigen-Specific Autoreactive B Cells in Sjögren's Disease: Methodological Challenges and Emerging Strategies.},
journal = {International journal of rheumatic diseases},
volume = {29},
number = {6},
pages = {e70728},
doi = {10.1111/1756-185x.70728},
pmid = {42252893},
issn = {1756-185X},
}

@article {pmid42255261,
year = {2026},
author = {Morris, SM and Pilat, K and Girard, EJ and Noll, A and Ang, LS and Price, J and Mhyre, AJ and Correnti, CE and Bandaranayake, AD and Mehlin, C and Clarke, M and Brasel, K and Muthuraman, P and Crook, ZR and Cole, B and Hylkema, TA and Le, Q and Meshinchi, S and Olson, JM},
title = {Fully human anti-FOLR1 T-cell engager demonstrates potent activity in CBFA2T3::GLIS2 acute megakaryoblastic leukemia.},
journal = {Blood neoplasia},
volume = {3},
number = {3},
pages = {100232},
pmid = {42255261},
issn = {2950-3280},
}

@article {pmid42079255,
year = {2026},
author = {Pravica, M and Franić, D and Bazdan, M and Guzalić, D and Bedalov, A and Boban, M},
title = {Proteasome-dependent degradation and nucleus-vacuole junctions sustain proteostasis during acute glucose starvation.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
doi = {10.64898/2026.04.22.720209},
pmid = {42079255},
issn = {2692-8205},
abstract = {How protein quality control is maintained during acute metabolic stress remains poorly understood. In budding yeast, abrupt glucose depletion rapidly lowers ATP levels and leads to the formation of chaperone-containing inclusions, suggesting that ATP-dependent degradation of misfolded proteins may be compromised when energy becomes limiting. Here we find that selective degradation of misfolded proteins remains active during acute glucose starvation despite reduced cellular ATP levels. Using model misfolded substrates in yeast Saccharomyces cerevisiae, we show that misfolded proteins continue to be efficiently degraded throughout both early and late phases of acute glucose depletion. This degradation requires the proteasome and depends on its functional 19S regulatory particle, indicating that ATP-dependent proteasomal activity persists during metabolic stress. We further find that nucleus-vacuole junctions (NVJs) promote efficient degradation during prolonged glucose starvation, revealing a role for organelle contact sites in supporting proteostasis under energy limitation. Together, these findings indicate that cells preserve proteasome-mediated proteostasis during acute glucose starvation, while NVJ membrane contact sites help sustain degradation capacity when metabolic resources are scarce.},
}

@article {pmid42146360,
year = {2026},
author = {Nemani, K and Jaycox, JR and Akcan, U and Schuman, BM and Yeon, SM and Harano, N and Qin, K and Notestine, AA and Carroll, SM and McKenzie, BS and Furchtgott, L and Lahti, AC and Tsien, RW and Agalliu, D and Goff, DC and Ring, AM},
title = {High prevalence of CNS-directed autoantibodies in patients with schizophrenia.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
pmid = {42146360},
issn = {2692-8205},
abstract = {Schizophrenia is a severe neuropsychiatric disorder whose etiology and biological heterogeneity remain poorly understood. Immune dysregulation has long been implicated, but the breadth and clinical significance of autoantibody responses remain unclear beyond rare individual examples. Here we use Rapid Extracellular Antigen Profiling-a proteome-scale assay for autoantibodies against extracellular and secreted proteins-to profile 352 individuals with schizophrenia and 971 community controls. We find that schizophrenia is marked by a striking elevation in extracellular autoantibody burden, present near disease onset, and approaching nearly twice control levels in the most severely ill patients. This burden increases with age in a pattern that diverges from controls and targets central nervous system antigens, including neuroactive receptors, neuronal ion channels, proteins involved in synaptic function, and blood-brain barrier integrity. Autoantibodies against blood-brain barrier antigens impair barrier function ex vivo and are associated with broader central nervous system autoreactivity, supporting a model in which barrier disruption promotes loss of tolerance to brain antigens. At the clinical level, higher baseline autoantibody burden predicts reduced responsiveness to the antipsychotic risperidone, suggesting that autoantibodies contribute to treatment resistance. Together, these findings identify humoral autoimmunity as a pervasive component of schizophrenia and imply that therapies that reset humoral immunity or reduce autoantibody burden may benefit patients beyond those with currently recognized antibody-mediated syndromes.},
}

@article {pmid42182320,
year = {2026},
author = {Deneke, VE and Suwita, JP and Wang, H and Tonai, S and Lu, Y and Panser, K and Schleiffer, A and Hollis, JA and Novatchkova, M and Dürnberger, G and Stejskal, K and Krssakova, G and Blaha, A and Andresan, AAR and Mirus, M and Marvanova, H and Chang, HY and Noda, T and Burga, A and Roitinger, E and Ikawa, M and Pauli, A},
title = {The SPARK complex forms the molecular basis of vertebrate fertilization.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
pmid = {42182320},
issn = {2692-8205},
abstract = {Fertilization requires gamete recognition and membrane fusion, yet the molecular basis of this process in vertebrates remains unknown. Here we identify SPARK (sperm protein assembly and receptor-binding key), a conserved multi-protein complex that integrates all known sperm fertilization factors, including TMEM81-IZUMO1-SPACA6 and DCST1/2, together with two newly identified components, TMDD1 and FAM187A. SPARK subunits are mutually dependent for stability in mature sperm, and disruption of any single component causes male sterility in zebrafish and mice. Incubating zebrafish sperm with soluble egg receptor Bouncer partially rescues fertilization of Bouncer-deficient eggs in a SPARK-dependent manner, consistent with egg receptor binding priming the complex for fusion. Thus, we propose SPARK as a conserved molecular machine that couples gamete recognition to membrane fusion.},
}

@article {pmid42244105,
year = {2026},
author = {Misono, S and Fann, JR and Osazuwa-Peters, N and Marmor, S},
title = {Mental Health and Survival in Medicare Beneficiaries With Lung and Head and Neck Cancer.},
journal = {Psycho-oncology},
volume = {35},
number = {6},
pages = {e70510},
pmid = {42244105},
issn = {1099-1611},
abstract = {BACKGROUND: Mental health (MH) conditions can significantly influence cancer outcomes, yet associations with survival and potential impacts of MH care utilization remain underexplored.

AIMS: Examine associations between (1) MH diagnoses and (2) MH utilization and survival among Medicare beneficiaries with lung or head and neck (HN) cancers.

METHODS: Patients diagnosed with lung or HN cancers between 2004 and 2018 were stratified by MH diagnosis status in the two years prior to cancer diagnosis. We examined factors associated with MH diagnosis and MH services and evaluated overall and cancer specific survival analyses using Kaplan-Meier survival analyses and multivariable Cox regressions.

RESULTS: 19% of patients with a lung cancer diagnosis (n = 333,875) and 15% of HN patients (n = 39,253) received a MH diagnosis within two years before cancer diagnosis. Kaplan-Meier survival analysis indicated significantly worse survival among patients with a MH diagnosis and higher rates of survival among those receiving MH services. Among individuals with a MH diagnosis, the mortality hazard for individuals that received MH services was lower compared to those who did not receive MH services, in both HN and Lung cancer.

CONCLUSIONS: MH conditions were common in people with lung and HN cancers and associated with worse overall and cancer-specific survival for head and neck cancer. Among those with MH diagnoses, receipt of MH services was associated with lower hazard of death, highlighting the need for early identification of this at-risk population and integration of MH care into oncology care.},
}

@article {pmid42244233,
year = {2026},
author = {Okello, P and Thuo, N and Roche, SD and Saravis, AL and Mwai, D and Naik, P and Kiptinness, C and Kareithi, T and Mugambi, ML and Sharma, M and Ngure, K and Ortbald, KF},
title = {Qualitative Insights on Client and Provider Barriers and Facilitators to Using a Novel Online HIV Pre- and Post-Exposure Delivery Model in Kenya.},
journal = {Journal of the International AIDS Society},
volume = {29},
number = {6},
pages = {e70133},
pmid = {42244233},
issn = {1758-2652},
support = {INV-037646/GATES/Gates Foundation/United States ; },
abstract = {INTRODUCTION: Online delivery of HIV pre- and post-exposure prophylaxis (PrEP and PEP) could address persistent access barriers, yet implementation across Africa remains limited. The ePrEP Kenya Pilot (NCT05377138) integrated PrEP and PEP services into an existing e-pharmacy platform and identified client- and provider-level barriers and facilitators to use.

METHODS: In the pilot, clinicians screened adults (age 18+) in Nairobi and Mombasa Counties for PrEP and PEP eligibility via telehealth; pharmaceutical technologists courier-delivered HIV testing services (including self-testing) and dispensed PrEP or PEP to eligible clients who paid 150-250 KES (∼$1-2 USD) for HIV testing, ≤149 KES (∼$1 USD) for courier delivery and nothing for telehealth consultation or PrEP/PEP drugs. We conducted monthly check-in calls with providers and, near study endline, in-depth interviews (IDIs) with purposively sampled clients and all providers. We analysed verbatim call transcripts and IDIs inductively, then mapped identified barriers and facilitators to the Consolidated Framework for Implementation Research (CFIR).

RESULTS: From February to November 2023, we conducted 10 check-in calls and interviewed 30 clients (10 PEP, 10 PrEP with 1+ refill, 10 PrEP with no refills) and 10 providers (4 clinicians, 6 pharm techs). Clients had a median age of 27 years (IQR 25-30) and providers 28 years (IQR 27-31); 53% (16/30) of clients and 30% (3/10) of providers were female. In the Outer Setting CFIR domain, providers identified motorcycle manoeuvrability as a delivery facilitator but noted that traffic, poor road infrastructure, bad weather and personal safety concerns posed challenges. In the Inner Setting domain, providers identified information-sharing practices and collegiality as facilitators. In the Individuals domain, clients' capability, opportunity and motivation to use online PrEP/PEP services was reportedly facilitated by app-guided HIV self-testing, broad delivery zones and enhanced privacy, but hindered by low awareness of these services, limited access to internet-enabled devices, data security concerns and uncertainties around couriers' pharmacy credentials. Recommendations included reducing client costs, expanding delivery coverage and hours, and offering alternative delivery options (e.g. medication pick-up lockers).

CONCLUSIONS: Online PrEP and PEP delivery is a promising differentiated service model, especially if partially subsidized by third-party payers. Implementation success will require model adaptations that address logistical, infrastructural and awareness barriers.},
}

@article {pmid42244408,
year = {2026},
author = {Loroña, NC and LaBrie, S and Thomas, CE and Yin, H and Huyghe, JR and Qu, C and Thomas, S and Nayemi, S and Ammar, H and Kahsai, O and Hsu, L and Curtis, KR and Koehne, A and Redwood, DG and Li, L and Li, CI and Peters, U and Thomas, TK and Phipps, AI and Figueiredo, JC and Hullar, M},
title = {Site- and age-dependent associations between Fusobacterium nucleatum and colorectal cancer mortality.},
journal = {Cancer},
volume = {132},
number = {12},
pages = {e70484},
doi = {10.1002/cncr.70484},
pmid = {42244408},
issn = {1097-0142},
support = {S10OD028685//Office of Research Infrastructure Programs, National Institutes of Health/ ; //GSF/ ; SR-202221337//M.J. Murdock Charitable Trust/ ; //V Foundation for Cancer Research/ ; P20CA252733/NH/NIH HHS/United States ; P30 CA015704/NH/NIH HHS/United States ; P50CA285275/NH/NIH HHS/United States ; R01CA155101/NH/NIH HHS/United States ; R01CA238087/NH/NIH HHS/United States ; R01CA248931/NH/NIH HHS/United States ; R01CA280639/NH/NIH HHS/United States ; R01CA284732/NH/NIH HHS/United States ; T32CA094880/NH/NIH HHS/United States ; U01CA290673/NH/NIH HHS/United States ; },
abstract = {BACKGROUND: Fusobacterium nucleatum (Fn) is a bacterium typically found in the human oral cavity that has been implicated in the development and progression of colorectal cancer (CRC).

OBJECTIVE: This study examines the association between prevalence of Fn in tumor tissue and CRC-specific mortality in a heterogeneous United States population.

METHODS: The present study includes 233 participants with stage I-III CRC who died of CRC, matched to 458 participants with CRC who did not die from their disease, within the Translational Research Program in Cancer Differences across Populations. Genomic DNA was extracted from formalin-fixed paraffin-embedded tumor tissue samples. Droplet digital polymerase chain reaction was used to assess the prevalence of Fn. The authors fit logistic regression models for the association between Fn positivity and CRC-specific mortality, adjusting for age, year of diagnosis, sex, stage, tumor site, population group, and tumor macrodissection status.

RESULTS: Presence of Fn in CRC tumor tissue was associated with 79% greater odds (95% CI, 1.20-2.67) of CRC-specific mortality. This association was more pronounced in participants with rectal (odds ratio [OR], 7.73; 95% CI, 2.13-34.79) than proximal colon (OR, 1.17; 95% CI, 0.65-2.08) or distal colon tumors (OR, 1.51; 95% CI, 0.74-3.04, p value for interaction = .023), and more pronounced with respect to early-onset (age <50 years; OR, 10.30; 95% CI, 2.09-70.53) than later-onset CRC (age ≥50 years; OR, 1.51; 95% CI, 0.98-2.33, p value for interaction = .010).

CONCLUSIONS: These findings support an association between presence of Fn in CRC tumor tissue and CRC-specific mortality, particularly for rectal tumors and early-onset CRC, in a heterogeneous population.},
}

@article {pmid42245734,
year = {2026},
author = {Zhang, JS and Ng, JCK and Hermida de Viveiros, P and Al-Marayaty, R and Al Akoum, N and Shinglot, H and Jing, W and Vizcaino, V and Alexiev, BA and Cranmer, LD and Loggers, ET and Abrams, H and Wagner, MJ and Pillarisetty, VG and Kim, EY and Pierce, RH and Berglund, P and Jones, RL and Lu, H and Ter Meulen, J and Pollack, SM and Seo, YD},
title = {Intratumoral TLR4 agonist therapy elicits antigen-specific T cell clonal expansion in metastatic leiomyosarcoma: a case series.},
journal = {Frontiers in oncology},
volume = {16},
number = {},
pages = {1829331},
pmid = {42245734},
issn = {2234-943X},
abstract = {Metastatic soft tissue sarcomas (STSs) are a heterogeneous group of rare mesenchymal tumors whose treatment options are limited. Our group has been interested in utilizing the synthetic toll-like receptor 4 (TLR4) agonist, glycopyranosyl lipid A in stable-emulsion formulation (GLA-SE), in patients with advanced STSs. Here, we report a case series of three patients with metastatic leiomyosarcoma who had superficial lesions amenable to intratumoral (IT) injection. We explored the safety, tolerability, and immunologic effects of IT GLA-SE given at 20 μg weekly for 12 weeks, both alone and in combination with radiotherapy. In this small case series, treatment was well tolerated, with no serious adverse events observed. Clinically, although no patient had significant tumor shrinkage, two had notable stability in their target lesions despite systemic disease progression. Immunologically, IT GLA-SE induced a clonal expansion of T cells intratumorally in one patient and in peripheral blood in another, suggesting an antitumor effect both at the site of injection and systemically. Moreover, GLA-SE elicited clonal expansion of systemic T cells targeting a well-known immunogenic cancer antigen, NY-ESO-1. The augmented expression of T cells targeting NY-ESO-1 in the systemic circulation of our patient following IT-GLA-SE warrants further investigation, given the promising role of NY-ESO-1 in current and future T-cell based immunotherapies. Together, these findings demonstrate the potential of IT GLA-SE to elicit antigen-specific T cell clonal expansion as a component of immunotherapeutic strategies to combat metastatic STSs. Expanded studies are needed to explore the clinical and immunologic effects of IT GLA-SE, particularly in combination with other immunotherapies.},
}

@article {pmid42248140,
year = {2026},
author = {DeWitt, WS and Vora, AA and Araki, T and Galloway, JG and Alkutkar, T and Bortolatto, J and Castro, TBR and Dumm, W and Jennings-Shaffer, C and Jia, T and Mesin, L and Ozorowski, G and Pae, J and Ralph, DK and Bloom, JD and Nourmohammad, A and Song, YS and Ward, AB and Starr, TN and Matsen, FA and Victora, GD},
title = {Replaying germinal center evolution on a quantified affinity landscape.},
journal = {Cell},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.cell.2026.05.013},
pmid = {42248140},
issn = {1097-4172},
abstract = {Darwinian evolution of immunoglobulin genes within germinal centers (GCs) underlies the progressive increase in antibody affinity following antigen exposure. Whereas the cellular mechanics of how competition between B cells increases affinity are well established, the evolutionary dynamics of this process are less clear. We developed an experimental evolution model in which we "replay" over one hundred monoclonal GC reactions, assigning affinities to each cell using deep mutational scanning. Our data reveal how GCs achieve predictable outcomes by means of noisy but persistent selection on an affinity landscape whose exploration is heavily constrained by somatic hypermutation biases. We infer a fitness landscape that quantitatively recapitulates the affinity maturation trajectory of our clone and find that apparent features of GC selection, such as permissiveness to low-affinity lineages and rapid plateauing of affinity, are likely artifacts of survivorship biases that distort our view of how B cell affinity progresses over time.},
}

@article {pmid42249080,
year = {2026},
author = {Budillon, A and Lemmers, RJLF and Tapscott, SJ and van der Maarel, SM},
title = {The emergence and diversification of the DUX gene family across placental mammals.},
journal = {Communications biology},
volume = {},
number = {},
pages = {},
doi = {10.1038/s42003-026-10442-2},
pmid = {42249080},
issn = {2399-3642},
support = {R01AR045203//Foundation for the National Institutes of Health (Foundation for the National Institutes of Health, Inc.)/ ; },
abstract = {The DUX gene family encodes transcription factors with paired homeodomains. It has critical roles in embryogenesis and disease, including facioscapulohumeral muscular dystrophy (FSHD) and cancer. This study conducts a comparative analysis of the DUX gene family-DUXA, DUXB (including DUXBL), and DUXC (including DUX4 and Dux)-across placental mammals, highlighting their structural diversity within macrosatellite repeat contexts. Using long-read genomes, we explore gene distribution, array patterns, and phylogenetic relationships in various vertebrate species. Our analysis reveals that DUXA and DUXB are highly conserved, with intriguing variations such as intronless forms likely arising from ancestral retrotransposition events. While DUXBL is inconsistently retained across clades, its locus-which in non-placental mammals harbors the ancestral single-homeodomain sDUX gene-served as an evolutionary hub for diversification, giving rise to DUXA, DUXB and DUXC, as well as macrosatellite tandem array structures. Sequence conservation and syntenic analyses demonstrate array adaptability, exemplified by higher-order repeats in orangutans and disrupted patterns of concerted evolution in elephants. Furthermore, analysis of human pseudo-DUX4 arrays indicates their potential role in disease mechanisms, including as possible contributors to rare cases of FSHD, warranting further investigation. This study thus provides insights into DUX-family gene evolution, offering a foundation for future research into developmental roles and disease implications.},
}

@article {pmid42243439,
year = {2026},
author = {Chestnut, C and McKoy, T and Westphalen, AC and Lin, DW and Nyame, YA},
title = {The clinical utility of prostate MRI before biopsy.},
journal = {Nature reviews. Urology},
volume = {},
number = {},
pages = {},
pmid = {42243439},
issn = {1759-4820},
abstract = {Approximately 1 in 8 men are diagnosed with prostate cancer during their lifetime. However, long-term data have shown that as many as half of diagnosed prostate cancers have low lethal potential. Early detection of prostate cancer relying on PSA alone is associated with potential harm to patients owing to false-positive results, prostate biopsy-related complications and over-detection and over-treatment of low-risk cancers. Multiparametric MRI offers an adjunctive strategy for improving the diagnostic yield of prostate biopsy and also for potentially reducing the need for biopsy in selected patients. Prostate MRI can increase the detection of clinically significant prostate cancer through targeted biopsy, especially in patients with a previous negative biopsy who did not undergo initial imaging. Prostate MRI improves clinically significant cancer detection, potentially reducing biopsy burden in patients on active surveillance.},
}

@article {pmid42241708,
year = {2026},
author = {Meyer, LK and Ryan, K and Panetta, JC and Crews, KR and Albeituni, S and Degar, BA and Hermiston, ML and Talano, JM and Torno, LL and Zambidis, ET and Trone, DJ and Sabin, ND and Maron, G and Flerlage, T and Thomas, PG and Cheng, C and Campbell, PK and Nichols, KE and Hines, MR},
title = {HLHRUXO: A prospective trial of a ruxolitinib-containing regimen for children with hemophagocytic lymphohistiocytosis.},
journal = {Blood advances},
volume = {},
number = {},
pages = {},
doi = {10.1182/bloodadvances.2026020265},
pmid = {42241708},
issn = {2473-9537},
abstract = {Hemophagocytic lymphohistiocytosis (HLH) is a severe hyperinflammatory syndrome characterized by excessive immune cell activation and hypersecretion of inflammatory cytokines, many of which signal via the Janus kinases (JAKs). Preclinical studies have demonstrated that the JAK1/2 inhibitor ruxolitinib ameliorates disease manifestations and prolongs survival in mouse models of HLH. Similarly, clinical studies have suggested that ruxolitinib is safe and effective for children with HLH, although prospective trials evaluating optimal ruxolitinib doses in primary (i.e., inherited/genetic) HLH are lacking. To address this gap, we developed HLHRUXO (https://clinicaltrials.gov/study/NCT04551131), a prospective multi-institutional clinical trial utilizing a ruxolitinib-containing regimen in children with newly diagnosed or relapsed/refractory HLH. Patients received ruxolitinib 25 mg/m2 twice daily combined with dexamethasone, with or without etoposide, for eight weeks, followed by continuation therapy at the discretion of the treating physician. Pharmacokinetic studies were performed on days one and eight. Eight patients (average age 7.6 years; five primary HLH [pHLH] and three secondary HLH [sHLH]) completed the study; none experienced dose-limiting adverse events (AEs). All patients experienced a favorable response at one week, demonstrating clinical stabilization and improvement in serum ferritin levels. Further, all five patients (three pHLH, two sHLH) with newly diagnosed HLH achieved a complete response (CR) after eight weeks of treatment, and all were alive at one year. One patient with relapsed/refractory sHLH achieved a CR at eight weeks and was alive at one year, while two others with relapsed/refractory pHLH died. Our findings confirm the safety of this ruxolitinib-containing regimen for pediatric HLH, with the best results observed in patients with newly diagnosed disease. Further studies of ruxolitinib as frontline therapy for children with HLH are warranted.},
}

@article {pmid42242253,
year = {2026},
author = {Fan, BE and Lam, BD},
title = {Artificial intelligence triage tool for bone marrow fibrosis in myeloproliferative neoplasms using complete blood counts.},
journal = {The Lancet. Haematology},
volume = {13},
number = {6},
pages = {e355-e357},
doi = {10.1016/S2352-3026(26)00129-8},
pmid = {42242253},
issn = {2352-3026},
}

@article {pmid42242398,
year = {2026},
author = {Rivas-Nieto, AC and Alver, SK and Mooney, SJ and Mossavar-Rahmani, Y and Xue, X and Lash, JP and Kaplan, R},
title = {Physical Activity Patterns and Kidney Function Changes Among Hispanic/Latino Adults: The Hispanic Community Health Study/Study of Latinos.},
journal = {Journal of physical activity & health},
volume = {},
number = {},
pages = {1-10},
doi = {10.1123/jpah.2025-0918},
pmid = {42242398},
issn = {1543-5474},
abstract = {BACKGROUND: Physical activity (PA) may be a modifiable factor for chronic kidney disease (CKD) prevention, but evidence specific to Hispanic/Latino populations is limited. Our objective was to examine associations between PA type/volume with changes in kidney function among Hispanic/Latino adults.

METHODS: We included participants (mean age: 41.6 years, 55.2% women) in the Hispanic Community Health Study/Study of Latinos with complete data. PA was measured using both 7-day accelerometry and the Global Physical Activity Questionnaire. Primary outcomes were percent change in estimated glomerular filtration rate (eGFR) and percent change in urine albumin-to-creatinine ratio over a mean of 6.1 years (N = 7071); incident CKD was the secondary outcome (N = 7177).

RESULTS: The mean eGFR change was -3.6 mL/min/1.73 m2, and mean urine albumin-to-creatinine ratio change was 4.0 mg/g. In multivariable-adjusted models accounting for demographic, occupational, and clinical factors, neither accelerometer-measured light PA or moderate to vigorous PA (MVPA) nor self-reported MVPA were significantly associated with changes in eGFR, urine albumin-to-creatinine ratio, or incident CKD (P > .05). Diabetes status significantly modified associations between eGFR percent change and accelerometer-measured light PA (interaction P < .01), MVPA (interaction P = .02), and self-reported total MVPA (interaction P = .03). Among individuals with diabetes, higher self-reported total MVPA was associated with higher eGFR change (0.12% per 15 min/d; 95% CI, 0.02-0.22), whereas greater accelerometer-measured MVPA was linked to higher CKD risk (incidence rate ratio: 1.12; 95% CI, 1.02-1.23). Among those without diabetes, associations were inverse with 95% CIs that overlapped the null.

CONCLUSIONS: PA types/volumes were not associated with kidney function decline or CKD incidence, though diabetes status may modify these relationships.},
}

@article {pmid42242424,
year = {2026},
author = {Arnold, DE and Eissa, H and Dunn, E and Cuvelier, GDE and Wright, NAM and Marsh, RA and Parikh, S and Saldana, BD and Vander Lugt, MT and Bacchetta, R and Satter, LF and Chandrakasan, S and Kellner, E and Allenspach, EJ and Schmitt, EG and Logan, B and Burroughs, L and Cowan, MJ and Griffith, LM and Notarangelo, L and Pai, SY and Pulsipher, MA and Dvorak, CC and Haddad, E and Puck, JM and Torgerson, TR and Leiding, JW and Heimall, J and Chan, AY},
title = {IMPACT (Immune Monitoring and Phenotype Assessment of Clinical Trajectory) for Patients with Inborn Errors of Immunity from the Primary Immune Deficiency Treatment Consortium (PIDTC).},
journal = {The journal of allergy and clinical immunology. In practice},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.jaip.2026.05.025},
pmid = {42242424},
issn = {2213-2201},
abstract = {BACKGROUND: Evaluating natural history and outcomes of rare inborn errors of immunity (IEIs) has been challenging due to the diverse disease manifestations and lack of standardized data.

OBJECTIVE: We developed a set of standardized, quantitative, generalizable data collection modules to measure organ dysfunction in IEIs, modeled on the previously validated Common Terminology Criteria for Adverse Event (CTCAE) system for grading treatment toxicity.

METHODS: Disease conditions were organized by organ system. Experts from the Primary Immune Deficiency Treatment Consortium (PIDTC) identified essential features of severe combined immunodeficiency (SCID), chronic granulomatous disease (CGD), Wiskott-Aldrich syndrome (WAS), and primary immune regulatory disorders (PIRD) and compared these to CTCAE conditions, adding and refining features as needed. Dates of onset and resolution, disease-specific laboratory values, and therapeutic interventions were also incorporated. Modules were reviewed by protocol teams, key stakeholders, clinical coordinators and statisticians to improve feasibility and completeness.

RESULTS: We developed a tool called IMPACT (Immune Monitoring and Phenotype Assessment of Clinical Trajectory) containing 15 modules assessing 196 disease conditions. A grading system from 1 to 5 (mild, moderate, severe, life-threatening, fatal) permits longitudinal tracking of disease condition severity. Outcomes of interventions can be measured quantitatively by comparing scores before and after treatment.

CONCLUSION: Standardized, quantitative assessment tools for IEIs can yield uniform datasets to illuminate their natural history and evaluate outcomes of interventions, not only to understand specific diseases, but also to compare effects between disease entities. Tools, like IMPACT, are essential for therapeutic trials for rare, complex multisystem diseases like IEIs and other disorders with protean manifestations.},
}

@article {pmid42242633,
year = {2026},
author = {Goldstein, CE and Armond, ACV and Cobey, KD and Voldal, EC and Chen, Y and Tingley, K and Shaw, JF and Heagerty, PJ and Hemming, K and Kenny, A and Li, F and Ouyang, Y and Xia, F and Moher, D and Hughes, JP and Taljaard, M},
title = {Data sharing in stepped-wedge cluster randomized trials: suboptimal data availability despite "data available upon request".},
journal = {Journal of clinical epidemiology},
volume = {},
number = {},
pages = {112353},
doi = {10.1016/j.jclinepi.2026.112353},
pmid = {42242633},
issn = {1878-5921},
abstract = {BACKGROUND: Data sharing enhances transparency, facilitates reproducibility, and promotes innovation in health research. For statisticians, access to data from real trials is essential to develop, validate, and refine statistical methods.

OBJECTIVES: Within a collection of published stepped-wedge cluster randomized trials (SW-CRTs), we aimed to describe the prevalence and types of data sharing statements; the actual availability of data after emailing authors; and factors associated with data obtainment.

METHODS: We identified SW-CRTs published between 2016-2022 from a previous systematic review and updated that search to include studies published through 31 December 2023. Data sharing statements, when provided, were classified as indicating data were publicly available, available upon request, or not available. Authors were emailed to request datasets. Associations between trial characteristics and data obtainment were explored using bivariable logistic regression and results reported as Odds Ratio (OR) with 95% Confidence Interval (CI).

RESULTS: Of 217 SW-CRTs identified, 98 (45%) had no clear data sharing statements, 89 (41%) indicated data were available upon request, 16 (7%) indicated data were not available, and 14 (7%) indicated data were publicly available. Datasets were ultimately obtained for 76 (35%) SW-CRTs. Data obtainment did not differ between studies with no data sharing statement and those indicating data were available upon request (both 34%). The odds of data obtainment were significantly higher among trials conducted in low- and middle-income countries (OR=2.9, 95% CI 1.5-5.4). The odds of data obtainment increased with years since publication (OR=1.13; 95% CI 0.99-1.29) and years since trial initiation (OR=1.11; 95% CI 1.00-1.23) although confidence intervals overlapped with the null. There was no clear evidence of an association with having positive primary trial results (OR=0.62; 95% CI 0.35-1.10), nor with journal impact factor, trial size, type of design, region of corresponding author, and funding source.

CONCLUSION: Data sharing practices in SW-CRTs are suboptimal. The presence of a data sharing statement is not predictive of actual data availability. There is significant regional variation in whether data were obtained but few other characteristics explain variation in data obtainment. Clear guidance and dedicated resources to facilitate data sharing in research are required.},
}

@article {pmid42242864,
year = {2026},
author = {Jiang, F and Shen, Y and Li, B and Henry, M and Davidson, N and Huang, Y},
title = {Inhibition of histone demethylase LSD1 suppresses CD47 expression and enhances efficacy of CD47 blockade in breast cancer.},
journal = {Journal for immunotherapy of cancer},
volume = {14},
number = {6},
pages = {},
doi = {10.1136/jitc-2025-014681},
pmid = {42242864},
issn = {2051-1426},
abstract = {BACKGROUND: CD47 functions as a "don't eat me" checkpoint, inhibiting macrophage-mediated phagocytosis in triple-negative breast cancer (TNBC). While anti-CD47 therapies can restore immune surveillance, their efficacy in TNBC is often limited by immune evasion and drug development challenges.

METHODS: We investigated the crosstalk between the histone demethylase lysine-specific demethylase 1 (LSD1) and CD47 signaling in TNBC using in silico datasets, isogenic cell lines, conditional BRCA1 knockout models, and syngeneic mouse models. Techniques such as immunohistochemistry, multiplex immunofluorescence, immunoprecipitation, protein ubiquitination, chromatin immunoprecipitation, chemotaxis, flow cytometry, and phagocytosis assays were employed to examine the epigenetic regulation of CD47 by LSD1 and its impact on antitumor immunity. The efficacy of combining LSD1 inhibition with anti-CD47 therapy was evaluated in BALB/cJ mice bearing TNBC tumors.

RESULTS: In TNBC tumors, CD47 expression is positively correlated with elevated LSD1 levels, which are associated with increased infiltration of M2 macrophages and a concomitant decrease in M1 macrophages and CD8+T cells. Inhibition of LSD1 led to downregulation of CD47 by suppressing the expression and activity of its key transcriptional regulators, NF-κB (p65) and STAT3, through distinct mechanisms. Loss of LSD1 reduced p65 transcription, which was linked to an accumulation of the repressive histone mark H3K9me2 at the p65 promoter. Conversely, LSD1 inhibition promoted polyubiquitination and subsequent destabilization of STAT3. LSD1 inhibition also enhanced phagocytosis and promoted M1 polarization of macrophages. CD47 downregulation induced the production of interferon-γ and Th1-type chemokines in TNBC cells, facilitating increased tumor infiltration of CD8+T cells. Furthermore, combining LSD1 inhibition with anti-CD47 therapy significantly improved antitumor efficacy compared with monotherapy in syngeneic tumor models, without inducing significant toxicity. This combination therapy also promoted a shift in macrophage polarization toward the M1 phenotype, further enhancing CD8+T cell infiltration within tumors. Depletion of CD8+T cells significantly diminished the antitumor efficacy of the combination therapy.

CONCLUSION: Targeting LSD1 enhances the efficacy of anti-CD47 therapy by overcoming immune evasion, offering a promising strategy to improve immunotherapy outcomes in TNBC.},
}

@article {pmid42233964,
year = {2026},
author = {Del Vecchio, NJ and Doria-Rose, VP and Todd, KW and Rendle, KA and Chubak, J and Halm, EA and Alonge, OD and Issaka, RB and Neslund-Dudas, C and Honda, S and Ziebell, RA and Li, CI and Zheng, Y and Hughes, AE and Ritzwoller, DP and Corley, DA},
title = {Impacts of a Public Health Emergency on Cancer Testing Rates, Follow-up, and Cancer Diagnosis: an Evaluation of the COVID-19 Pandemic.},
journal = {Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology},
volume = {},
number = {},
pages = {},
doi = {10.1158/1055-9965.EPI-26-0292},
pmid = {42233964},
issn = {1538-7755},
abstract = {BACKGROUND: Public health emergencies can substantially impact routine healthcare. Large cancer screening declines during the early months of the COVID-19 pandemic are well-documented; however, COVID-19's impact on follow-up of abnormal screening exams and cancer diagnoses is less reported. We examined the impacts of COVID-19 on the cervical, colorectal, and lung cancer screening processes, within 10 health systems in the Population-based Research to Optimize the Screening Process (PROSPR) consortium.

METHODS: PROSPR data were used to calculate: (1) monthly rates of cancer testing and, for pre-COVID and COVID time periods, (2) proportions of individuals receiving recommended follow-up within 6 months of an abnormal test, and (3) cancer incidence. Surveys were used to assess the healthcare systems' local context.

RESULTS: During the first two months of the pandemic, cancer testing decreased across all health systems and cancer types (range18-96%). Overall, decreases in monthly rates were followed by rapid recovery to pre-pandemic rates. The rates of 6-month follow-up of abnormal screening results trended down in the COVID vs. pre-COVID periods, as did the diagnosis of new cancers.

CONCLUSIONS: Declines in cancer testing in the early months of the COVID-19 pandemic were short-term, with at least short-term impacts on diagnostic follow-up and cancer diagnosis. The systems with the smallest decreases were those that both utilized remote screening outreach (e.g., mailed FIT kits) and did not pause that outreach at the start of the pandemic.

IMPACT: Strategies and policies implemented by healthcare systems during public health emergencies can help minimize disruptions in care.},
}

@article {pmid42234759,
year = {2026},
author = {Naffeti, BS and Ayoub, HH and Johnston, C and Abu-Raddad, LJ},
title = {Projected public health benefits of a hypothetical HSV-1 vaccine in the United States: A mathematical modeling analysis.},
journal = {Science advances},
volume = {12},
number = {23},
pages = {eaee0698},
pmid = {42234759},
issn = {2375-2548},
mesh = {Humans ; *Herpesvirus 1, Human/immunology ; United States/epidemiology ; *Models, Theoretical ; *Herpes Simplex Virus Vaccines/immunology ; *Public Health ; *Herpes Simplex/prevention & control/epidemiology/immunology ; Vaccination ; Female ; Adolescent ; Infant ; },
abstract = {Herpes simplex virus type 1 (HSV-1) infection is highly prevalent worldwide and causes oral, genital, and neonatal herpes. Several HSV vaccine candidates are currently in development. This study used mathematical modeling to estimate the potential population-level impact of HSV-1 vaccination strategies in the United States. Infant vaccination with 70% efficacy and lifelong protection introduced in 2030 reduced oral and genital incidence rate by 47.3 and 58.3% by 2075, respectively, with annual new infections declining by 41.2 and 53.5%, corresponding to 28.5 million cumulative infections averted. The number needed to vaccinate to prevent one infection, defined from program initiation to a specified year, declined from 35.8 by 2040 to 7.2 by 2070. Addition of adolescent catch-up vaccination further reduced oral and particularly genital incidence. Lifelong protection produced approximately threefold greater impact than 15-year protection. HSV-1 vaccination could substantially reduce oral and genital HSV-1 burden, supporting prioritization of vaccine development and integration into public health strategies.},
}

Humans
*Herpesvirus 1, Human/immunology
United States/epidemiology
*Models, Theoretical
*Herpes Simplex Virus Vaccines/immunology
*Public Health
*Herpes Simplex/prevention & control/epidemiology/immunology
Vaccination
Female
Adolescent
Infant

@article {pmid42234933,
year = {2026},
author = {Doroshow, DB and Leal, TA and Waqar, SN and Borghaei, H and Camidge, DR and Dragnev, KH and Edelman, MJ and Gandara, DR and Gerber, DE and Gray, JE and Hirsch, FR and Husain, H and Kozono, DE and Leighl, NB and Li, BT and Mack, PC and Neal, JW and Paik, PK and Patel, SP and Riess, JW and Redman, MW and Reckamp, KL},
title = {Resistance to Immune Checkpoint Inhibitor Treatment in Non-Small Cell Lung Cancer Clinical Trials: A Perspective From Lung-MAP Investigators.},
journal = {Journal of clinical oncology : official journal of the American Society of Clinical Oncology},
volume = {},
number = {},
pages = {JCO2501896},
doi = {10.1200/JCO-25-01896},
pmid = {42234933},
issn = {1527-7755},
}

@article {pmid42235031,
year = {2026},
author = {Annamalay, A and Radich, J},
title = {Chronic Myeloid Leukemia in Low- and Middle-Income Countries. Reply.},
journal = {The New England journal of medicine},
volume = {394},
number = {21},
pages = {2175-2176},
doi = {10.1056/NEJMc2605636},
pmid = {42235031},
issn = {1533-4406},
}

@article {pmid42236300,
year = {2026},
author = {Andrews, H and Agnihotram, R and Blumenthal, G and Bullock, J and Collins, G and Doherty, GJ and Farago, AF and Ishii, Y and Kasichayanula, S and LeBlanc, M and Levi-D'Ancona, E and Li, C and McCullough, K and Morrow, PK and Navarro, B and Sandhu, P and Shah, S and Sharon, E and Su, Z and Vallett, C and Villalobos, Y and Allen, JD and Stewart, MD},
title = {Assessing Contribution of Effect in Oncology Combination Therapies: Lessons Learned to Inform and Optimize Future Registrational Trial Designs.},
journal = {The oncologist},
volume = {},
number = {},
pages = {},
doi = {10.1093/oncolo/oyag222},
pmid = {42236300},
issn = {1549-490X},
abstract = {Combination therapies can be used to significantly improve clinical outcomes in patients undergoing treatment for cancer, however, they also present challenges when establishing the contribution of effect (COE) for each component. Although factorial trials remain the most rigorous approach for determining COE, they are often impractical, such as in settings with rare cancers, aggressive disease, evolving standards of care, or monotherapy components with limited activity. As more combination regimens are co-developed from the outset, alternative approaches to registrational trial designs are needed to balance scientific rigor with feasibility and patient acceptability. Thoughtfully designed alternative approaches can support an understanding of COE when grounded in prior evidence and mechanistic understanding. Four major categories of evidence emerge to support designing combination trials without factorial arms: (1) data from trials of the same combination in other tumor types; (2) data from trials of agents with similar mechanisms of action; (3) data from early-phase or parallel trials of the combination within the same disease setting; and (4) strong mechanistic or clinical evidence that a monotherapy component lacks activity and/or imposes harm, supporting omission of inactive arms. Early regulatory engagement, prespecified decision rules, and transparent justification of design choices are essential to ensure that combination regimens provide meaningful improvement in efficacy over monotherapies while minimizing unnecessary toxicity. Applying these principles to combination therapy development can maximize patient benefit while maintaining scientific rigor.},
}

@article {pmid42237020,
year = {2026},
author = {Richards, AR and Gomez, MF and Dowling, BI and Bulka, CM and Gigic, B and Figueiredo, JC and Li, CI and Shibata, D and Toriola, AT and Byrd, DA and Ulrich, CM and Teng, M and Stewart, PA and Siegel, EM and Kresovich, JK},
title = {Abundance and balance of circulating leukocyte subsets and colorectal cancer survival.},
journal = {British journal of cancer},
volume = {},
number = {},
pages = {},
pmid = {42237020},
issn = {1532-1827},
abstract = {BACKGROUND: Cancer immunology research has traditionally focused on tumor-infiltrating leukocytes, but the role of the peripheral leukocytes remains understudied. Since tumor-infiltrating leukocytes are recruited from the blood, circulating immune profiles may provide prognostic insights obtainable before surgery, reflecting overall immune competence.

METHODS: We analyzed treatment-naïve blood samples from 134 stage I-III colorectal cancer (CRC) patients using a nested case-control design (33 recurrences, 45 deaths; median follow-up: 7.4 years). Circulating leukocyte subsets were estimated using methylation cytometry applied to genome-wide methylation profiles. Cox regression models estimated associations between leukocyte metrics and disease-free and overall survival, adjusting for clinical factors.

RESULTS: Higher counts of circulating neutrophils and T-regulatory cells were associated with worse disease-free and overall survival (neutrophil, disease-free HR: 1.32, 95% CI: 1.01, 1.72, P = 0.04; overall HR: 1.39, 95% CI: 1.00, 1.94, P = 0.05; T regulatory, disease-free HR: 1.32, 95% CI: 1.00, 1.74, P = 0.05; overall HR: 1.38, 95% CI: 1.00, 1.90, P = 0.05). Memory B cells were associated with worse disease-free survival (HR: 1.56, 95% CI: 1.31, 1.86, P < 0.0001), particularly in those diagnosed with rectal cancer. Higher basophil counts and proportions were associated with worse overall survival (count HR: 1.44, 95% CI: 1.05, 1.99, P = 0.02; proportion HR: 1.47, 95% CI: 1.06, 2.03, P = 0.02), with stronger associations in those diagnosed at earlier stages or with rectal tumors.

CONCLUSIONS: Peripheral immune cell composition identifies CRC patients at higher risk for recurrence and death, providing insights into systemic immune contributions to CRC survival.},
}

@article {pmid42237094,
year = {2026},
author = {Lim, MY and Gangaraju, R and Jafari, O and Yang, Z and Tiong, JWT and Chiang, ECL and Ma, S and Jiang, JY and Ryu, J and Lam, BD and Ranjan, M and Li, A},
title = {Clinically Relevant Bleeding in Individuals With Cancer: Insights From a Nationwide Cohort Study.},
journal = {American journal of hematology},
volume = {},
number = {},
pages = {},
doi = {10.1002/ajh.70394},
pmid = {42237094},
issn = {1096-8652},
support = {R01 HL180402/NH/NIH HHS/United States ; K23 HL159271/NH/NIH HHS/United States ; K08 HL159290/NH/NIH HHS/United States ; RR190104//Cancer Prevention and Research Institute of Texas/ ; ASH Scholar Award//American Society of Hematology/ ; Career Development Award//Conquer Cancer Foundation/ ; },
abstract = {Cancer care is often complicated by coagulopathy leading to thrombosis and bleeding. While venous thromboembolism (VTE) has been extensively studied, bleeding remains an underestimated threat. To address this knowledge gap, we leveraged the Epic Cosmos database to determine the impact of cancer-associated clinically relevant bleeding (CRB) in 2 455 332 individuals with incident cancer encounters from 215 US health systems between 2018 and 2024. In the 12 months leading up to the cancer diagnosis, the period prevalence of CRB was 5.3% in the overall cohort, highlighting CRB as a common early presentation preceding cancer diagnosis. In the 12-month window after cancer diagnosis, the cumulative incidence of CRB was 6.3% in the overall cohort, 7.0% in those receiving systemic antineoplastic therapy, and up to 15.0% among individuals on certain baseline anticoagulants. In addition to age, sex, and race, factors appreciably associated with CRB on multivariable analysis included cancer types, metastatic disease, systemic therapy, anticoagulant or antiplatelet use, higher comorbidity index, recent hospitalization, recent history of bleeding or VTE, and selective laboratory features (hemoglobin, platelets, albumin, eGFR). Furthermore, the onset of CRB as a time varying covariate was independently associated with mortality in multivariable adjusted analysis: intracranial hemorrhage (HR 4.17, 95% CI 4.11-4.24); gastrointestinal bleeding (HR 2.52, 95% CI 2.50-2.55); other bleeding (HR 2.46, 95% CI 2.44-2.49). Together, these findings reveal a substantial and overlooked risk of bleeding in cancer care and underscore a need for validated bleeding risk models that can be integrated alongside VTE prediction tools to guide personalized thromboprophylaxis decisions.},
}

@article {pmid42237652,
year = {2026},
author = {Abramson, JS and Siddiqi, T and Gordon, LI and Lunning, MA and Wang, M and Arnason, JE and Kamdar, M and Maloney, DG and Shadman, M and Andreadis, CB and Sehgal, A and Solomon, SR and Ghosh, N and Hidalgo-López, JE and Wang, J and Ding, X and Ogasawara, K and Singh, A and Palomba, ML},
title = {Five-year survival outcomes from TRANSCEND NHL 001 of lisocabtagene maraleucel in R/R LBCL.},
journal = {Blood},
volume = {},
number = {},
pages = {},
doi = {10.1182/blood.2025032270},
pmid = {42237652},
issn = {1528-0020},
abstract = {We present 5-year survival results in patients with R/R LBCL from TRANSCEND NHL 001 (TRANSCEND), including data from the separate long-term follow-up (LTFU) study. Overall, 345 patients were leukapheresed, 270 received liso-cel, and 257 were efficacy evaluable. Among efficacy-evaluable patients, median overall survival (OS) was 27.5 months (95% confidence interval [CI], 16.2‒47.3; leukapheresed set, 15.2 months [95% CI, 11.5‒23.4]) with estimated 5-year OS rate of 38% (95% CI, 32‒45; leukapheresed set, 33% [95% CI, 28‒39]). Median disease-specific survival (DSS; excludes deaths unrelated to disease progression) was 67.8 months (95% CI, 23.5‒not reached [NR]; leukapheresed set, 27.4 months [95% CI, 14.4‒69.7]) with estimated 5-year DSS rate of 52% (95% CI, 45‒59; leukapheresed set, 47% [95% CI, 41‒52]). Among efficacy-evaluable patients from TRANSCEND who were alive at end-of-study and enrolled in the LTFU (n=84), median OS and DSS were NR (95% CI, NR‒NR) and estimated 5-year OS and DSS rates were 78% (95% CI, 67‒86) and 92% (95% CI, 84‒97), respectively. Most deaths occurred ≤2 years after infusion; no new safety signals were observed with low rates of late severe infections and second primary malignancies. These data support the curative potential of liso-cel in patients with R/R LBCL. Clinicaltrials.gov: NCT02631044, NCT03435796.},
}

@article {pmid42237892,
year = {2026},
author = {Connerty, P and Colgan, JN and El-Najjar, F and Henry, E and Xie, J and Idais, D and Gentile, C and Mao, J and Dolman, MEM and Marshall, GM and Lock, RB},
title = {The myeloid cell leukaemia-1 inhibitor MIK665 is a potent therapy in preclinical models of paediatric acute myeloid leukaemia.},
journal = {British journal of haematology},
volume = {},
number = {},
pages = {},
doi = {10.1111/bjh.70596},
pmid = {42237892},
issn = {1365-2141},
support = {RSP-655-FY2023//Tour de Cure/ ; RSP-023-2017//Tour de Cure/ ; RRE/0700:SZ//Anthony Rothe Memorial Trust/ ; 1157871//National Health and Medical Research Council/ ; //Heart Research Australia/ ; //Perpetual IMPACT/ ; //Catholic Archdiocese of Sydney/ ; //Heart Research Institute/ ; },
abstract = {Paediatric acute myeloid leukaemia (AML) remains a deadly disease, with survival rates reaching a plateau despite treatment with high-intensity chemotherapy. Recent advancements in therapeutic strategies, such as targeted therapies to inhibit AML dependencies, have aimed to improve outcomes. The evasion of apoptosis, regulated by the B-cell lymphoma 2 (BCL2) family of proteins, is a key feature of cancer progression and treatment resistance. Bcl-2 homology domain 3 (BH3) mimetics, such as venetoclax (ABT-199), which targets BCL2, have shown promising activity in AML. This study investigates for the first time the therapeutic potential of MIK665, a BH3 mimetic targeting myeloid cell leukaemia-1 (MCL1), in paediatric AML. We evaluated the efficacy of MIK665 against a diverse panel of AML cell lines and demonstrated its effectiveness as a single-agent treatment. Additionally, MIK665 showed significant activity against a subset of paediatric AML patient-derived xenografts (PDXs) in both ex vivo and in vivo experiments, with minimal impact on cardiac tissue pathophysiology. These findings strongly support the clinical advancement of MIK665 for paediatric AML treatment in a precision medicine approach.},
}

@article {pmid42238104,
year = {2024},
author = {Hudson, A and Geng, EH and Odeny, TA and Bukusi, EA and Petersen, ML and van der Laan, MJ},
title = {An approach to nonparametric inference on the causal dose-response function.},
journal = {Journal of causal inference},
volume = {12},
number = {1},
pages = {},
pmid = {42238104},
issn = {2193-3677},
abstract = {The causal dose-response curve is commonly selected as the statistical parameter of interest in studies where the goal is to understand the effect of a continuous exposure on an outcome. Most of the available methodology for statistical inference on the dose-response function in the continuous exposure setting requires strong parametric assumptions on the probability distribution. Such parametric assumptions are typically untenable in practice and lead to invalid inference. It is often preferable to instead use nonparametric methods for inference, which only make mild assumptions about the data-generating mechanism. We propose a nonparametric test of the null hypothesis that the dose-response function is equal to a constant function. We argue that when the null hypothesis holds, the dose-response function has zero variance. Thus, one can test the null hypothesis by assessing whether there is sufficient evidence to claim that the variance is positive. We construct a novel estimator for the variance of the dose-response function, for which we can fully characterize the null limiting distribution and thus perform well-calibrated tests of the null hypothesis. We also present an approach for constructing simultaneous confidence bands for the dose-response function by inverting our proposed hypothesis test. We assess the validity of our proposal in a simulation study. In a data example, we study, in a population of patients who have initiated treatment for HIV, how the distance required to travel to an HIV clinic affects retention in care.},
}

@article {pmid42240813,
year = {2026},
author = {Mandrik, O and Thomas, C and Bessey, A and Brennan, A and Carvalho, AL and Castilla-Rodríguez, I and Doroshenko, O and Hill, H and Kunst, N and Nagy, B and Payne, K and Pollard, D and Ramsey, SD and Roitberg, F and Shinkins, B and Smith, RA and Thom, H and Whyte, S},
title = {Correction: Ten Recommendations for Modelling Cost Effectiveness of Screening: Perspectives of an International Stakeholder Group.},
journal = {PharmacoEconomics},
volume = {},
number = {},
pages = {},
doi = {10.1007/s40273-026-01627-y},
pmid = {42240813},
issn = {1179-2027},
}

@article {pmid42240981,
year = {2026},
author = {Quandt, Z and Othus, M and Sharon, E},
title = {Fluids for Immune Checkpoint Inhibitor Diabetic Ketoacidosis-Reply.},
journal = {JAMA oncology},
volume = {},
number = {},
pages = {},
doi = {10.1001/jamaoncol.2026.1589},
pmid = {42240981},
issn = {2374-2445},
}

@article {pmid42241697,
year = {2026},
author = {Sorror, ML and Artz, AS},
title = {Implementing CHARM in Transplant Practice.},
journal = {Blood advances},
volume = {},
number = {},
pages = {},
doi = {10.1182/bloodadvances.2026020708},
pmid = {42241697},
issn = {2473-9537},
}

@article {pmid42227161,
year = {2026},
author = {Cardamone, LM and Prasad, P and Croix, M and Seidenfeld, A and Heldman, M and McConn, K and Mulanovich, V and Liakos, ADP and Koo, S and Chemaly, RF and Boeckh, M and Yoke, LH},
title = {Immunocompromised Host Infectious Diseases: A Recommended Educational Content Outline for Advanced Practice Providers.},
journal = {Transplant infectious disease : an official journal of the Transplantation Society},
volume = {},
number = {},
pages = {e70252},
doi = {10.1111/tid.70252},
pmid = {42227161},
issn = {1399-3062},
}

@article {pmid42227732,
year = {2026},
author = {Deng, Y and Wang, R and Zhang, T and Zhan, X},
title = {Randomized Interventional Effects in Semicompeting Risks, With Application to a Hematopoietic Cell Transplantation Study.},
journal = {Statistics in medicine},
volume = {45},
number = {13-14},
pages = {e70628},
doi = {10.1002/sim.70628},
pmid = {42227732},
issn = {1097-0258},
abstract = {In clinical studies, the risk of the primary (terminal) event may be modified by intermediate events, resulting in semicompeting risks. To study the treatment effect on the terminal event mediated by the intermediate event, researchers wish to decompose the total effect into direct and indirect effects. In this article, we extend the randomized interventional approach to time-to-event outcomes, where both intermediate and terminal events are subject to right censoring. We envision a random draw for the intermediate event process from a reference distribution, either marginally over time-varying confounders or conditionally given the observed history. We present the identification formula for interventional effects. We also discuss some variants of the identification assumptions. We estimate the treatment effects using nonparametric maximum likelihood estimation and propose a sensitivity analysis that incorporates a latent frailty. As an illustration, we study the effect of matched unrelated donor versus haploidentical donor on death mediated by relapse in a hematopoietic cell transplantation study with graft-versus-host disease (GVHD) as the time-varying confounder. We find that matched unrelated donor transplantation is preferable in terms of survival rates under the use of post-transplant PTCy GVHD prophylaxis for lymphoma patients.},
}

@article {pmid42229584,
year = {2026},
author = {Francis, PA and Pagani, O and Fleming, GF and Walley, BA and Colleoni, M and Rubovszky, G and Tondini, C and Ciruelos, EM and Gomez, HL and Bonnefoi, HR and Burstein, HJ and Chini, C and Puglisi, F and Spazzapan, S and Bernardo, A and Climent, MA and Bellet, M and Ruhstaller, T and Bermejo, B and Chia, SKL and Martino, S and Geyer, CE and Goetz, MP and Ingle, JN and Stearns, V and Davidson, NE and Le Du, F and Müller, B and Coleman, RE and Loibl, S and Winer, EP and Ruepp, B and Loi, S and Láng, I and Coates, AS and Gelber, RD and Goldhirsch, A and Regan, MM and , and , },
title = {Final outcomes of the SOFT and TEXT phase III trials in premenopausal hormone receptor-positive early breast cancer.},
journal = {Annals of oncology : official journal of the European Society for Medical Oncology},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.annonc.2026.05.704},
pmid = {42229584},
issn = {1569-8041},
abstract = {BACKGROUND: The SOFT trial found adding ovarian function suppression (OFS) to tamoxifen (T) reduced breast cancer recurrence, and exemestane (E)+OFS further reduced recurrence. SOFT and TEXT combined analysis showed a significant reduction in distant recurrence with E+OFS versus T+OFS. We now report final 15-year outcomes.

PATIENTS AND METHODS: Premenopausal women with hormone receptor-positive early breast cancer were enrolled, with 3047 in SOFT and 2660 in TEXT intention-to-treat populations. SOFT randomized to 5 years of T versus T+OFS versus E+OFS. TEXT randomized to 5 years of T+OFS versus E+OFS. Chemotherapy was optional, prior to SOFT entry with subsequent premenopausal oestradiol, or concurrent with OFS in TEXT. Endpoints included disease-free survival, breast cancer-free interval (BCFI), distant recurrence-free interval (DRFI) and overall survival. 15-year Kaplan-Meier estimates, hazard ratios (HR) and 95% confidence intervals (CI) are reported.

RESULTS: In SOFT, escalating endocrine therapy (ET) continued to reduce recurrence with 15-year BCFI 78.6% for E+OFS, 75.7% for T+OFS and 72.1% for T; T+OFS versus T, HR 0.82 (CI 0.69-0.98) P=0.03. In the SOFT no-chemotherapy cohort, OFS reduced breast cancer events at 15 years, while DRFI and overall survival remained high regardless of ET assignment. After prior chemotherapy for HER2-negative tumours (n=1257), SOFT 15-year overall survival was 81.0% with E+OFS versus 77.1% with T+OFS versus 76.8% with T. In women under age 35 with HER2-negative tumours (n=241), 15-year overall survival was 82.5% with E+OFS, 77.9% with T+OFS and 68.1% with T. In combined SOFT and TEXT analysis, among those with HER2-negative tumours (n=4035), E+OFS versus T+OFS reduced distant recurrence HR 0.75 (CI 0.63-0.90), with a smaller reduction in deaths HR 0.89 (CI 0.74-1.06), with absolute survival benefits largest with high-risk features, particularly young age or high-grade tumours.

CONCLUSION: Meaningful overall survival benefit in hormone receptor-positive, HER2-negative breast cancer from adjuvant exemestane and/or OFS compared with tamoxifen alone is limited to high-risk premenopausal subgroups. Tamoxifen-based ET may not result in optimal outcomes in premenopausal high-grade HER2-negative tumours.},
}

@article {pmid42229633,
year = {2026},
author = {Dacic, S and Shenker, D and Redman, M and Brunner, L and Saqi, A and Cooper, WA and Borczuk, A and Chung, JH and Glass, C and Lopez, JM and Roden, AC and Sholl, L and Weissferdt, A and Brosnan-Cashman, J and Hennek, S and Grullon, S and Posadas, J and Fujimoto, J and Connolly, C and Wynes, MW and Sanchez-Espiridion, B and Lee, JJ and Berezowska, S and Chou, TY and Kerr, K and Nicholson, AG and Schalper, KA and Tsao, MS and Ready, N and Cascone, T and Heymach, J and Sepesi, B and Shu, C and Rizvi, N and Sonett, J and Altorki, N and Provencio, M and Bunn, PA and Kris, MG and Travis, W and Yu, L and Wistuba, I and , },
title = {Machine learning assessment of pathologic response in lung cancer resections after neoadjuvant therapy - IASLC MPR Project.},
journal = {Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer},
volume = {},
number = {},
pages = {103953},
doi = {10.1016/j.jtho.2026.103953},
pmid = {42229633},
issn = {1556-1380},
abstract = {INTRODUCTION: Machine learning algorithms may improve efficiency and accuracy of pathologic response (PR) assessment in surgically resected lung cancers following neoadjuvant therapy. The aim of this study was to develop digital models for quantifying tumor bed (TB) area and residual viable tumor (VT), and to compare these results to previously published assessments of PR by pathologists from the IASLC reproducibility study.

METHODS: Manual pathologist annotations (N=15,564) of regions including TB and VT were used to train convolutional neural network model (digital AI) and a Convex Hull algorithm (CHA). PR was determined by the percentage of VT in the TB area. The pathologist determined the average PR (APR) across slides (unweighted) which was compared to the weighted average for digital AI and CHA. The concordance between pathologist APR, digital AI and CHA was calculated, and correlated with outcomes.

RESULTS: There was a strong correlation between approaches: APR vs. Digital AI (0.97), APR vs. CHA (0.97), and Digital AI vs. CHA (0.99). Digital PR and CHA showed 100% agreement for MPR. The kappa concordance for MPR was 0.82 (95% CI: 0.69, 0.96) for APR versus Digital AI/CHA with 6 discordant cases. The concordance was higher for squamous cell carcinoma (Kappa 0.92, 95% CI: 0.76, 1.0) than for non-squamous carcinoma (Kappa 0.77, 95% CI: 0.59, 0.96). APR and digital AI showed similar relapse-free survival (RFS) and overall survival (OS).

CONCLUSION: The overall high level of agreement supports the utility of the machine learning approaches for evaluations of PR in patients with NSCLC.},
}

@article {pmid42230962,
year = {2026},
author = {Arrieta-Bolaños, E and Lima, ACM and Andreani, M and De Santis, D and Malard, F and Mayor, NP and Mehta, RS and Meisel, R and Pagliuca, S and Petersdorf, E and Piemontese, S and Sacchi, N and Santoro, N and Sanz, J and Schetelig, J and Spellman, SR and Onida, F and Sánchez-Ortega, I and Mohty, M and Yakoub-Agha, I and Fleischhauer, K and Ruggeri, A},
title = {HLA matching in contemporary haematopoietic cell transplantation: Recommendations from the EBMT Practice Harmonisation and Guidelines Committee.},
journal = {Bone marrow transplantation},
volume = {},
number = {},
pages = {},
pmid = {42230962},
issn = {1476-5365},
abstract = {HLA compatibility has been a cornerstone for safe and successful allogeneic haematopoietic cell transplantation (HCT), with human leukocyte antigen (HLA)-mismatched transplants consistently associated with inferior survival. However, recent advances in typing technologies, supportive care, and novel graft-versus-host disease (GvHD) prophylaxes have prompted the revisiting of HLA mismatch relevance in contemporary HCT. Within the framework of the 3[rd] Workshops of the Practice Harmonization & Guidelines Committee, the EBMT convened a group of experts in histocompatibility & immunogenetics, HCT immunobiology, and clinical HCT, to review the current state of the art and develop a set of consensus-based recommendations on the role of HLA in current HCT. The topics included technological aspects of HLA typing, the role of HLA mismatches in donor selection, and the detection and management of anti-HLA antibodies in HLA-mismatched transplantation. Moreover, the role of HLA matching relative to other non-HLA factors and in the context of novel GvHD prophylaxes, non-malignant disease, and pediatric populations was defined. Finally, the relevance of special models for HLA matching and of post-HCT monitoring of HLA-loss in malignant disease relapse was reviewed. The present document summarizes the expert consensus on these topics, to provide evidence-based recommendations for clinical decision-making.},
}

@article {pmid42232582,
year = {2025},
author = {Mugwanya, KK and Matemo, D and Meisner, A and Schaafsma, T and Morton, J and Wandera, C and Kemunto, V and Cherotich, I and Odhiambo, S and Bii, M and Oduor, B and Achieng, E and Oyombra, T and Owaga, D and Beima-Sofie, KM and Baeten, JM and Kinuthia, J},
title = {Integrating oral pre-exposure prophylaxis delivery in primary care family planning clinics: a pragmatic, stepped-wedge, cluster-randomised trial.},
journal = {The Lancet. Primary care},
volume = {1},
number = {5},
pages = {},
pmid = {42232582},
issn = {3050-5143},
abstract = {BACKGROUND: Integrating pre-exposure prophylaxis (PrEP) delivery in family planning (FP) settings may offer an efficient platform to reach women at elevated risk for HIV.

METHODS: We conducted a stepped-wedge cluster randomized trial to integrate systematic screening for HIV risk and PrEP delivery in twelve public FP clinics in Kisumu County, Kenya. Clients were HIV-negative women 15-49 years accessing the participating clinics. Each clinic represented a cluster, and four clinics sequentially transitioned from usual care (control) to the intervention period in a randomized staged order every three-month interval. The intervention included provider training and technical support to build FP clinic staff capacity to deliver PrEP as part of the standard of care. There was no masking. Oral PrEP was free to clients. A subset of women assessed to be at elevated HIV risk including those who declined PrEP were enrolled in nested cohort and followed quarterly up to 24 months to measure HIV incidence. The primary outcomes were the proportion of women screened for oral PrEP among those attending FP clinics and PrEP initiation among women screened and assessed to be eligible for PrEP. Analysis was intention-to-treat, with all women not known to be living with HIV at the first clinic visit encounter included in the analysis for the HIV risk and PrEP screening outcome. This trial is registered with ClinicalTrials.gov., NCT04666792 and completed.

RESULTS: Between March 1, 2021 and December 31, 2022, 25457 HIV-negative women visited twelve FP clinics contributing 7386 woman-encounters during control period and 21343 woman-encounters during the intervention period. Median age was 27 (IQR 23-31) years. The proportion of woman-encounters screened for PrEP significantly increased from 2.9% (213/7386) to 91.6% (19560/21343) (relative risk: 20·5, 95%CI 3·5-120.4; p=0·0008). Oral PrEP initiation among women assessed to be at elevated HIV risk increased from 3.9% (5/120) to 40.6% (985/2429) (relative risk: 50·1, 95%CI 2·8-913.4; p=0·0082). Five HIV infections occurred during 833·4 women-years of cohort follow-up (incidence 0.60 95%CI 0.19-1.40 per 100 woman-years). All infections were in women who either declined PrEP (n=3) or had undetectable tenofovir diphosphate in dried blood spots at multiple visits prior to seroconversion (n=2).

INTERPRETATION: An implementation intervention package to build capacity of public clinic FP healthcare providers successfully led to integration of oral PrEP delivery in real-world FP clinics in Kenya. These findings could help inform similar strategies in FP clinics in other African settings.},
}

@article {pmid42232894,
year = {2026},
author = {Liu, Y and Carlson, C and Prajogi, GB and Jhingran, A and Holliday, E and Paly, J and Longo, J and Puckett, LL and Zaorsky, NG and Sarria, G and Castaneda, SA and Li, BC},
title = {A New Remote Classroom Approach to Contouring Training for Pelvic Malignancies in Low- to Middle-Income Asian Countries.},
journal = {Cureus},
volume = {18},
number = {4},
pages = {e108054},
pmid = {42232894},
issn = {2168-8184},
abstract = {BACKGROUND AND PURPOSE: The feasibility, learner interest, and educational impact of online contouring training in low- and middle-income countries (LMICs) in Asia have not been documented on a large participant scale; hence, we aimed to investigate these factors while conducting a training program in contouring pelvic malignancies.

MATERIALS AND METHODS: A 10-session contouring course was offered to primarily radiation oncologists in Southeast Asia (SEA) via Zoom (Zoom Communications, Inc., San Jose, USA). The curriculum included case-based learning and supplemental reading materials focusing on common contouring scenarios and errors. Participation and pre- and post-program surveys, including demographics, confidence scores, a 10-question contouring knowledge test, and anonymous feedback, were recorded and analyzed. Changes in pre- and post-program scores were evaluated using a paired t-test.

RESULTS: A total of 276 physicians participated in the curriculum, with 144 participants completing pre- and post-confidence score surveys and knowledge tests. The attendance for each session averaged 140 (range 115-158). Among paired participants, mean confidence scores increased from 2.92 to 3.67 out of 5 (+26.28%, p<0.01) and were significantly improved across all disease sites (range +21.5% to +34.1%). Mean knowledge test scores increased from 4.47 to 6.53 out of 10 (+46.2%, p<0.01). The average likelihood of recommending this training program to another colleague was 9.63 out of 10.

CONCLUSIONS:  The pelvic malignancies contouring training program, which focused on avoiding common errors, resulted in robust participation, significant improvements in confidence and knowledge scores, and excellent course recommendation scores. This strategy could potentially be replicated for continuous medical education, scaled to other countries, and applied to other cancer disease sites in the future.},
}

@article {pmid42233054,
year = {2026},
author = {Srinivasan, P and Bechtel, M and Wyczechowska, D and Ochoa, AC and Fisch, MJ and Henry, NL and Unger, JM and Hamilton-Reeves, JM},
title = {Flow cytometry method to identify arginase-1 expressing MDSCs.},
journal = {MethodsX},
volume = {16},
number = {},
pages = {103957},
pmid = {42233054},
issn = {2215-0161},
abstract = {Myeloid-derived suppressor cells (MDSCs) contribute to immune suppression in cancer through arginase-1 (ARG1), which limits T-cell activation. Conventional assays such as ELISA or qPCR cannot determine the cellular source of ARG1 in blood. Recognizing the importance of ARG1 in immunosuppression, we developed and validated a standardized flow cytometry method using a commercially available ARG1 antibody to measure intracellular ARG1 in MDSC subsets. This method includes detailed instructions, including experimental optimization using positive and negative controls, to help other researchers perform flow cytometric measurement of ARG1 expressing cells. In this method, peripheral blood mononuclear cells were stained for lymphoid and myeloid markers (CD3, CD20, CD56, HLA-DR, CD33, CD11b, CD14, and CD15), fixed, and permeabilized before intracellular ARG1 staining. Antibody specificity was verified using neutrophils as positive and CD4[+] T cells as negative controls. The method was applied to blood samples from patients with bladder cancer (n = 23) and healthy volunteers (n = 10), demonstrating reliable detection of intracellular ARG1 in MDSC subpopulations. This accessible protocol provides an adaptable method for quantifying cell-specific ARG1 expression and studying MDSC-mediated immunosuppression.•The flow cytometry method described here was developed by validating the arginase1 antibody binding specificity using cells expressing high and very low levels of arginase-1.•Arginase-1-expressing cells of the peripheral blood monocytes were identified using this method.•This method can be adapted to any cell type and will be a valuable tool in future immunosuppression studies.},
}

@article {pmid42233504,
year = {2026},
author = {Mamis, K and Bozic, I},
title = {Early-stage cancer results in a multiplicative increase in cell-free DNA originating from healthy tissue.},
journal = {Journal of the Royal Society, Interface},
volume = {23},
number = {239},
pages = {},
doi = {10.1098/rsif.2025.0349},
pmid = {42233504},
issn = {1742-5662},
support = {DMS-2045166//National Science Foundation/ ; //Pacific Institute for the Mathematical Sciences/ ; },
abstract = {Cell-free DNA (cfDNA) is a promising biomarker for cancer detection. However, the sources of elevated cfDNA in patients with early-stage cancer, and the mechanisms by which cfDNA is shed into, and subsequently cleared from the circulation are still poorly understood. Using a rich dataset of cfDNA in healthy individuals and early-stage cancer patients, we find a multiplicative increase in cfDNA concentration in the presence of cancer. This increase is cancer type-specific, ranging from an approximately 1.3-fold increase in lung cancer to an approximately 12-fold increase in liver cancer, and does not originate from the tumour, but from healthy tissue. Employing an additional dataset reporting the tissue of origin of cfDNA, we observe a significant increase in the correlation between cfDNA originating from leukocytes and from non-leukocyte sources in cancer patients. Introducing a mathematical model for cfDNA dynamics, we find that the observed correlation can be explained by a saturation mechanism in cfDNA clearance. Saturation in clearance implies that smaller increases in cfDNA shedding may lead to proportionally larger increases in cfDNA levels. Our findings quantify cfDNA dynamics in patients with cancer, with implications for improving the accuracy of liquid biopsies for early cancer detection.},
}

@article {pmid42233639,
year = {2026},
author = {Stearns, K and Marcink, T and Pawlack, E and Sobolik, EB and Porotto, M and Greninger, AL and Nieweisk, S and Moscona, A},
title = {Human parainfluenza virus 3 fusion protein cleavage: a key determinant of infection and spread.},
journal = {Journal of virology},
volume = {},
number = {},
pages = {e0212625},
doi = {10.1128/jvi.02126-25},
pmid = {42233639},
issn = {1098-5514},
abstract = {UNLABELLED: Human parainfluenza virus 3 (HPIV3) entry into target cells depends on a viral fusion complex composed of hemagglutinin-neuraminidase (HN) and fusion protein (F). In addition to attachment, HN activates F to mediate membrane fusion, while its neuraminidase activity promotes viral release. This creates a biological paradox: virions must repeatedly engage sialic acid-rich substrates in the airway without prematurely triggering F until they reach the target cell sialic acid receptor. Unlike the F proteins of laboratory strains that are cleaved intracellularly by furin to process F from its pro-protein to the active form that is essential for fusion, the F proteins of HPIV3 field strains lack a furin cleavage site and undergo partial cleavage mediated by extracellular serine proteases. We show that virions isolated directly from infected humans contain both cleaved and uncleaved F. In viral migration assays, reducing the proportion of cleaved F on virions increases the distance virions travel before infecting a cell. Even virions bearing only uncleaved F upon egress from infected cells can establish infection in vivo. These findings support a model in which uncleaved F on viral surfaces permits virions to engage and disengage sialylated substrates without undergoing premature fusion protein triggering, allowing virions to traverse the airway. Cleavage of F at the target cell then licenses membrane fusion, ensuring that virions initiate infection at the correct site. HPIV3 exploits host protease environments to produce virions with heterogeneity in F cleavage, equipped to either establish local infection or spread to distant target cells.

IMPORTANCE: Parainfluenza viruses employ their surface glycoproteins, the receptor-binding (hemagglutinin-neuraminidase) and fusion (F) proteins, to fuse with target cell membranes and infect the airway. F is made as an inactive precursor that is activated when host cell proteases cleave it to produce the fusion-competent form. Previous studies, utilizing laboratory-adapted viruses, assumed that F proteins are pre-cleaved on virus produced by infected people. We show that virions isolated directly from infected humans contain both cleaved and uncleaved F proteins. In viral migration assays, reducing the proportion of cleaved F on virions increases the distance virions travel before infecting a cell. The uncleaved F proteins enable virions to travel from their cell of origin without undergoing premature fusion protein activation, allowing virions to traverse the airway and infect the proper target cells. HPIV3 exploits host protease environments to produce a spectrum of virions suited to either local infection or intra-host spread.},
}

@article {pmid41860794,
year = {2026},
author = {Cunningham, D and Liu, J and Cevher Zeytin, I and de la Cerda, DA and Ghatwai, N and Courtney, AN and Guo, L and Rathi, P and Yao, CQ and Zhang, N and An, Z and Heczey, A},
title = {Coexpression of IL15 Promotes Effector Differentiation and Sustained Proliferative Capacity in ALPPL2-Specific Human CAR T Cells.},
journal = {Cancer immunology research},
volume = {14},
number = {6},
pages = {933-943},
doi = {10.1158/2326-6066.CIR-25-0609},
pmid = {41860794},
issn = {2326-6074},
support = {RP190561 & RP250465//Cancer Prevention and Research Institute of Texas (CPRIT)/ ; AU-0042-20030616//Welch Foundation (The Welch Foundation)/ ; //Texas Children's Hospital (TCH)/ ; //Seattle Children's Research Institute/ ; },
abstract = {Chimeric antigen receptor (CAR) T cells have robust antitumor activity against hematologic malignancies and have the potential to benefit patients with solid tumors. Immune recognition of murine proteins expressed in adoptively transferred T cells and the lack of homeostatic cytokines in the tumor microenvironment can limit the expansion and persistence of CAR T cells. CARs generated only from human sequences could reduce the risk of immune-mediated rejection, and interleukin 15 (IL15), which promotes T-cell survival and fitness, may improve the expansion and persistence of CAR T cells. In this study, we report a CAR construct (ABBz) assembled from human sequences including a single-chain variable fragment (scFv) specific to alkaline phosphatase, placental-like 2 (ALPPL2). This binder was selected through an unbiased, high-throughput screen of a human antibody-derived, phage-displayed scFv library based on binding specificity, stringency, and low dissociation constant. We demonstrated specificity to the antigen, effective cytolytic function, and cytokine production in ABBz T cells. We showed NK-like effector differentiation with sustained proliferative capacity specific to secreted IL15 coexpression in ABBz T cells. Lastly, we demonstrated that ABBz CAR T cells had robust antitumor activity, which was further enhanced through IL15 coexpression, resulting in NK-like effector differentiation with increased cytotoxicity and superior expansion capacity due to reduced apoptosis of CAR T cells. These results demonstrate that IL15 coexpression can promote effector differentiation while maintaining the proliferative capacity of huALPPL2-CAR T cells and provide a foundation for further clinical development of IL15-coexpressing huALPPL2-CAR T cells in patients.},
}

@article {pmid42218667,
year = {2026},
author = {Vasavada, A and Triplette, M and Palazzo, L and Ralston, J and Carter-Bawa, L and Luce, C and Green, BB and Gao, H and Anderson, ML and Su, YR and Rogers, K and Wernli, KJ},
title = {Is Anybody Out There? Understanding the Reach of Lung Cancer Screening Health Communication Through EHR Patient Portal.},
journal = {Journal of health communication},
volume = {},
number = {},
pages = {1-12},
doi = {10.1080/10810730.2026.2679491},
pmid = {42218667},
issn = {1087-0415},
abstract = {Health communication addressing individuals eligible for lung cancer screening (LCS) can increase screening uptake and adherence, which remain low in the U.S. Digital Communication via EHR patient portals offers a scalable solution, but face barriers related to portal access and use. We conducted a secondary analysis of a pragmatic clinical trial (Kaiser Permanente Washington, Nov 2022-Apr 2024) to identify gaps in access and engagement with an LCS health communication intervention delivered via portal message. We assessed factors associated with 1) patient portal access (all participants, n = 1837); and 2) opening the intervention message (intervention arm only, n = 820) using multivariate log binomial regression to calculate prevalence ratios (PRs) and confidence intervals (CIs). Most participants (89.6%) had access to the portal. No access was associated with current tobacco use (PR 0.4), neighborhood income <$50K (PR 0.3), and <5 years of insurance (PR 0.5). Among the intervention group, 81.2% opened the message. Not opening was associated with older age (PR 0.7), current tobacco use (PR 0.5), >1 well-care visit in the past year (PR 0.6), and 5-10 years of insurance (PR 0.5). While patient portals can broadly deliver LCS interventions, disparities in access and engagement suggest the need for alternative communication strategies.},
}

@article {pmid42224345,
year = {2026},
author = {Radtke, S and Laszlo, GS and Swing, K and Repele, A and Barton, JW and King, DJ and Pande, D and Enstrom, MR and Li, J and Wolf, CB and Reevey, L and Petty, NE and Kanestrom, G and Loeb, KR and Pettenger-Willey, CM and Othus, M and Kehret, AR and Cole, FM and Lunn-Halbert, MC and Hamlin, DK and Wilbur, DSS and Sandmaier, BM and Kiem, HP and Walter, RB},
title = {[211At]Astatine-Based Conditioning with a Humanized CD45 Antibody for Autologous Hematopoietic Stem Cell Gene Therapy.},
journal = {Blood},
volume = {},
number = {},
pages = {},
doi = {10.1182/blood.2026033789},
pmid = {42224345},
issn = {1528-0020},
abstract = {Successful transplantation of autologous gene-modified hematopoietic stem/progenitor cells (HSPCs) requires efficient ablation of resident hematopoietic stem cells. Since conventional myeloablative conditioning regimens are associated with non-hematologic toxicities, we evaluated CD45-directed radioimmunotherapy (RIT) using the a-emitter astatine-211 (211At) before transplantation of ex vivo gene-edited autologous HSPCs as an alternative in nonhuman primates. We humanized the CD45 antibody, BC8 (HuBC8), and labeled it with 211At. As a model, mobilized CD34+ HSPCs were multiplex gene-edited using an adenine base editor, modifying the HBG promoter to reactivate fetal hemoglobin (HbF) and deleting CD33. Two animals each received 300 or 400 µCi/kg of 211At. In contrast to historic controls conditioned with total body irradiation, CD45-RIT animals did not show any noticeable non-hematopoietic toxicities and were almost entirely transfusion independent with rapid recovery of neutrophils and platelets. 211At enabled dose-dependent engraftment of gene-edited cells. A new single cell sequencing assay revealed up to 70% combined mono- and bi-allelic gene-editing efficiency in the blood, consistent with complete replacement of the bone marrow stem cell compartment. Assessment by bulk analysis underestimated the frequency of gene-edited cells, highlighting the importance of a single cell readout. Single cell sequencing further confirmed stable and unbiased contribution of multiplex-edited HSPCs to all mature lineages in the blood, providing high-resolution data assuring successful replacement upon autologous HSPC gene therapy. Levels of edited cells remained stable for the entire follow-up of >18 months. Together, these studies identify 211At-CD45 RIT as a targeted alternative for myeloablative conditioning for autologous gene therapy.},
}

@article {pmid42224351,
year = {2026},
author = {Lin, Z and Gao, Y and Sun, W},
title = {Supervised deep learning with gene functional annotation for cell classification.},
journal = {PLoS computational biology},
volume = {22},
number = {6},
pages = {e1014327},
doi = {10.1371/journal.pcbi.1014327},
pmid = {42224351},
issn = {1553-7358},
abstract = {Gene-by-gene differential expression analysis is a widely used supervised approach for interpreting single-cell RNA-sequencing (scRNA-seq) data. However, modern scRNA-seq datasets often contain large numbers of cells, leading to the identification of many differentially expressed genes with extremely small p-values but negligible effect sizes, thus making biological interpretation difficult. To overcome this challenge, we developed Supervised Deep learning with gene functional ANnotation (SDAN), a method that integrates gene functional annotation information (e.g., protein-protein interaction) with gene-expression profiles through a graph neural network. SDAN identifies functionally coherent gene sets that optimally classify cells, and the resulting cell-level classification scores can be aggregated to make individual-level predictions. We evaluated SDAN alongside three representative existing methods in three real-data applications aimed at identifying gene sets associated with severe COVID-19, dementia, and cancer immunotherapy response. Across all applications, SDAN consistently outperformed the alternative approaches by achieving two objectives simultaneously: accurate outcome classification and clear assignment of genes to functionally related gene sets.},
}

@article {pmid42224356,
year = {2026},
author = {Macleod, D and Floyd, S and Shanaube, K and Probert, W and Bwalya, J and Schaap, A and Skalland, T and Moore, A and Piwowar-Manning, E and Hoddinott, G and Bond, V and Simwinga, M and Mandla, N and Donnell, D and Bock, P and Ayles, H and Fidler, S and Hayes, R and , },
title = {Migration and its impact on universal HIV testing and treatment in the HPTN 071 (PopART) study communities.},
journal = {PLOS global public health},
volume = {6},
number = {6},
pages = {e0005357},
doi = {10.1371/journal.pgph.0005357},
pmid = {42224356},
issn = {2767-3375},
abstract = {Migrants have been identified as a population left behind by the AIDS (Acquired Immune Deficiency Syndrome) response, with evidence showing poorer HIV (Human Immunodeficiency Virus) outcomes and reduced intervention effectiveness in mobile populations. We used data from the HPTN 071 (PopART) trial (ClinicalTrials.gov number, NCT01900977) to investigate migration and HIV-related indicators, assessing whether community migration influenced PopART trial results and whether migration was associated with HIV status and position on the care continuum. The PopART trial, conducted in Zambia and South Africa (SA) from November 2013 to June 2018, evaluated a universal testing and treatment intervention using a three-arm design. A cohort of 18-44-year-olds was followed annually to estimate HIV incidence, with migration out of trial communities tracked using this cohort. migration into and within the community was tracked using intervention delivery data in community members aged 18 + . HIV-related indicators were HIV status, knowledge of HIV-positive status and ART use. Migration's influence on the trial HIV incidence results was analysed using a two-stage approach for cluster-randomised trials, adjusting for community-level migration. Associations between HIV-related indicators and both out-migration (Poisson regression using cohort data) and in-migration (logistic regression using cross-sectional data) were also estimated. While migration differed between trial arms, there was no evidence that it confounded the intervention effect on HIV incidence. There was evidence out-migration was higher among HIV-positive individuals who did not know (or did not disclose) their HIV-positive status compared to those HIV-negative (adjusted rate ratio: Zambia 1.28, 95%CI 1.17-1.39; SA 1.27, 95%CI 1.17-1.38). Residents who had moved into the community within the previous year were less likely to be aware of their HIV-positive status than longer-term residents (adjusted odds ratio: Zambia 0.18, 95%CI 0.16-0.19; SA 0.23, 95%CI 0.20-0.28) and contributed to approximately one in four of the newly identified HIV infections. Following intervention delivery the gap in knowledge of HIV status and ART treatment coverage between recent in-migrants and longer-term residents closed. Countries with high HIV burden should aim to ensure a sustained delivery of HIV services in areas with high levels of population mobility and in areas with moderate to high HIV prevalence.},
}

@article {pmid42225836,
year = {2026},
author = {Chan, M and Ma, H and Subbiah, V and Gujral, TS},
title = {Mutation-centric kinase drug repurposing for rare cancers.},
journal = {Nature reviews. Cancer},
volume = {},
number = {},
pages = {},
pmid = {42225836},
issn = {1474-1768},
}

@article {pmid42124561,
year = {2026},
author = {Talavera, IC and Graham, JB and Swarts, JL and Traxinger, BR and Peters, MQ and Warrier, L and Koehne, AL and Arkatkar, T and Jerome, KR and Prlic, M and Lund, JM},
title = {Regulatory T cells restrain IL-15-mediated cytotoxic and bystander T cell activity in mucosal tissue without compromising antigen-driven memory.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
pmid = {42124561},
issn = {2692-8205},
abstract = {Many pathogenic human infections enter the host via a mucosal surface. These nonlymphoid tissues are abundantly populated by polyclonal memory CD8 T cells that persist following infections to protect the host in the event of repeat exposure. Memory T cells can be triggered via T cell receptor (TCR) interaction with their cognate antigen upon re-infection to exert effector functions, including cytotoxicity and cytokine production, and assist in pathogen elimination. Alternatively, some T cells are 'bystander activated' by cytokines without antigenic signal. This layered approach boosts efficient pathogen clearance but also poses a threat to host tissues if this response is not properly controlled. Here we investigate the regulatory mechanisms modulating the tissue memory CD8 T cell response upon recall, leveraging mouse models to distinguish antigen-driven versus cytokine-activated memory tissue CD8 T cell immunity. We find that regulatory T cells (Treg) play a role in restricting cytotoxic and bystander activity in mucosal T cells without compromising the antigen-driven protective memory CD8 T cell response. Critically, Treg provide extrinsic regulation of tissue CD8 T cell cytotoxicity through restriction of available IL-2 and IL-15 trans-presentation. Our findings help to define the extrinsic environmental and cellular cues in mucosal tissues that direct tissue memory CD8 T cell cytotoxicity.},
}

@article {pmid42147192,
year = {2026},
author = {Alexander, MW and Wood, B and See-Hwee Oh, H and Bot, VA and Borger, J and Galbiati, F and Walker, KA and Resnick, SM and Ochs-Balcom, HM and Wyss-Coray, T and Kooperberg, C and Reiner, AP and Jacobs, EG and Rabin, JS and Casaletto, KB and Saloner, R},
title = {Plasma proteomics link menopause timing to brain aging and dementia risk.},
journal = {Research square},
volume = {},
number = {},
pages = {},
pmid = {42147192},
issn = {2693-5015},
abstract = {Earlier menopause is a risk factor for several age-related diseases, including dementia. The biological pathways linking menopause timing to later-life brain aging are not understood. Leveraging large-scale plasma proteomics in postmenopausal women from the UK Biobank (N=15,012), earlier menopause was associated with upregulation of pro-inflammatory and extracellular matrix degradation pathways, plus accelerated aging across proteomic clocks of organ and cellular aging, including brain and oligodendrocyte aging. Elevated GDF15, a canonical aging marker, was the top protein correlate of earlier menopause. We observed robust replication of menopause timing proteomic shifts in the Women's Health Initiative Long Life Study (N=1,210). In UKB, proteins associated with earlier menopause, including GDF15, exhibited concordant associations with incident dementia risk and brain atrophy, cerebral small vessel disease burden, and white matter microstructural integrity. Collectively, our findings identify proteomic signatures linking ovarian aging to brain aging, providing a framework to inform interventions to reduce dementia risk.},
}

@article {pmid42213891,
year = {2026},
author = {Coghill, AE and Bender Ignacio, R},
title = {Further unraveling the association between HIV, immune suppression, and cancer survival.},
journal = {Clinical infectious diseases : an official publication of the Infectious Diseases Society of America},
volume = {},
number = {},
pages = {},
doi = {10.1093/cid/ciag334},
pmid = {42213891},
issn = {1537-6591},
}

@article {pmid42214050,
year = {2026},
author = {Gunn, CM and Boyer, N and Sheikh, S and Lee, JM and Woloshin, S and Specht, JM and Hubbard, RA and Aiello Bowles, EJ and Tosteson, ANA},
title = {Patient- and Physician-Identified Considerations for Clinical Implementation of a New Risk-Based Prediction Tool to Guide Surveillance Mammography in Breast Cancer Survivors.},
journal = {JCO oncology practice},
volume = {},
number = {},
pages = {OP2501048},
doi = {10.1200/OP-25-01048},
pmid = {42214050},
issn = {2688-1535},
abstract = {PURPOSE: Patient, tumor, and treatment factors can help predict the chance that a woman with a history of breast cancer diagnosis will be diagnosed with a second breast cancer within a year of a negative mammogram. This qualitative study elucidates breast cancer survivor and multispecialty physician perspectives on barriers/facilitators to clinical implementation of a risk-prediction tool to support surveillance decisions.

MATERIALS AND METHODS: We enrolled women who completed primary breast cancer treatment and physicians from November 2023 to April 2024. Participants were recruited through Breast Cancer Surveillance Consortium's registries; patients participated in one of four focus groups and physicians participated in individual semistructured interviews. Participants were presented with information about an interval cancer risk prediction tool and were prompted to share perspectives on facilitators and barriers to using such a tool. To identify salient themes, thematic analysis was undertaken by three research team members.

RESULTS: Participants included 40 physicians and 23 patients. Three themes emerged: (1) evidence needed for tool acceptance, (2) tool features to facilitate usage, and (3) barriers to tool adoption. Both cancer survivor and physician groups were accepting of risk prediction tool use for surveillance imaging when tool development information was available; they perceived the tool would fit within workflows, and data integrity could be verified. Both groups anticipated structural (time) and technological barriers (magnetic resonance imaging availability) could impede adoption.

CONCLUSION: Qualitative findings from focus groups and interviews analyzed thematically suggest implementing a risk prediction tool for surveillance imaging requires evidence transparency, health record integration, data integrity protection, and system supports to promote ease of use in clinical settings while mitigating unintended consequences. All are important to consider during tool development and implementation planning.},
}

@article {pmid42217442,
year = {2026},
author = {Brown, LG and Coleman, IM and Chu, TLH and Sayar, E and Patel, RA and Hanratty, B and Adil, M and Li, D and Li, Y and Nguyen, HM and Sessions, CJ and Sweeney, EL and Alumkal, JJ and da Costa, RMG and Wang, Y and Lin, DW and True, LD and Dumpit, R and Corey, E and Lee, JK and Nelson, PS and Xin, L and Haffner, MC and Morrissey, C},
title = {Systematic analysis of hippo pathway signaling identifies TEAD1 as a transcriptional regulator of neuroendocrine prostate cancer.},
journal = {Neoplasia (New York, N.Y.)},
volume = {78},
number = {},
pages = {101321},
doi = {10.1016/j.neo.2026.101321},
pmid = {42217442},
issn = {1476-5586},
abstract = {Treatment-induced neuroendocrine prostate cancer (NEPC) represents an aggressive form of castration-resistant prostate cancer (CRPC) associated with lineage plasticity and therapeutic resistance. In this study, we investigated the role of the Hippo signaling axis in the transdifferentiation from androgen receptor-positive prostate cancer (ARPC) to NEPC. RNA sequencing analyses of CRPC metastases revealed coordinated alterations in Hippo pathway components, with decreased expression of YAP1, LATS2, and TEAD2 and increased expression of LATS1, TEAD1, and the RNA splicing regulator RBFOX2 in NEPC. These transcriptional alterations were consistently observed across multiple model systems and patient samples. Epigenetic analyses demonstrated that reduced expression of YAP1, TEAD2, and LATS2 was associated with increased DNA methylation, whereas elevated TEAD1 expression correlated with DNA hypomethylation in NEPC. NEPC selectively retained TEAD1 expression, including a spliced isoform not detected in ARPC. Proteomic interactome analyses revealed that TEAD1 associated with RNA splicing factors and DNA repair proteins. Functional studies showed that TEAD1 knockdown led to the reversion of gene programs associated with epithelial differentiation. These findings indicate that the conversion of ARPC to NEPC involves coordinated loss of AR, YAP1, and REST activity alongside sustained TEAD1 expression and altered RNA processing. Our data identify TEAD1 as a transcriptional regulator associated with the NEPC state and suggest a role for TEAD1-linked transcriptional and post-transcriptional mechanisms in prostate cancer lineage plasticity.},
}

@article {pmid42218145,
year = {2026},
author = {Ping, J and Jia, G and Cai, Q and Guo, X and Wang, J and Tao, R and Li, B and Bauer, JA and Xie, Y and Ambs, S and Barnard, ME and Chen, Y and Choi, JY and Gao, YT and Garcia-Closas, M and Gu, J and Hu, JJ and Iwasaki, M and John, EM and Kweon, SS and Li, CI and Matsuda, K and Matsuo, K and Nathanson, KL and Nemesure, B and Olopade, OI and Pal, T and Park, SK and Park, B and Press, MF and Sanderson, M and Sandler, DP and Yao, S and Zheng, Y and Ahearn, T and Brewster, AM and Falusi, A and Hennis, AJM and Ito, H and Kubo, M and Lee, ES and Makumbi, T and Mapoko, BSE and Noh, DY and O'Brien, KM and Ojengbede, O and Olshan, AF and Park, MH and Reid, S and Yamaji, T and Zirpoli, G and Butler, EN and Huang, M and Low, SK and Obafunwa, J and Weinberg, CR and Zhang, H and Zhao, H and Ambrosone, CB and Cote, ML and Huo, D and Haiman, CA and Kang, D and Palmer, JR and Troester, MA and Shu, XO and Long, J and Zheng, W},
title = {Multi-ancestry transcriptome-wide association studies uncover insights into breast cancer genetics and biology.},
journal = {Nature communications},
volume = {},
number = {},
pages = {},
doi = {10.1038/s41467-026-73801-x},
pmid = {42218145},
issn = {2041-1723},
support = {R01CA235553//U.S. Department of Health & Human Services | National Institutes of Health (NIH)/ ; R01CA202981//U.S. Department of Health & Human Services | National Institutes of Health (NIH)/ ; R01CA148667//U.S. Department of Health & Human Services | National Institutes of Health (NIH)/ ; R01CA124558//U.S. Department of Health & Human Services | National Institutes of Health (NIH)/ ; },
abstract = {Genome-wide association studies (GWAS) have identified over 200 genetic risk loci for breast cancer, yet their target genes remain largely unknown. We conduct multi-ancestry transcriptome-wide association studies (TWAS) to discover potential breast cancer susceptibility genes. We develop ancestry-specific genetic models to predict levels of gene expression, alternative splicing, and 3' UTR alternative polyadenylation using genomic and transcriptomic data from 652 normal female tissue samples and apply these models to GWAS data of 178,534 cases and 248,300 controls for association analyses. We identify 290 genes associated with breast cancer risk, including 103 previously unreported and 46 not located at known GWAS loci, and 39 genes show distinct associations with breast cancer risk by estrogen-receptor status. Single-cell RNA sequencing and in vitro experiment data provide additional functional evidence for 169 genes. These genes are enriched in pathways implicated in breast carcinogenesis. Our study uncovers insights into breast cancer genetics and biology.},
}

@article {pmid42211136,
year = {2026},
author = {Rashidi, A and Minot, SS and Lee, SJ and Hill, GR and Podlesny, D},
title = {Cohesive modules of engraftment in fecal microbiota transplantation.},
journal = {iScience},
volume = {29},
number = {6},
pages = {116025},
pmid = {42211136},
issn = {2589-0042},
abstract = {While single-strain probiotics fail to address community-level microbiota injuries in dysbiosis-related conditions and fecal microbiota transplantation (FMT) produces unpredictable communities, a middle-ground approach has emerged. This approach involves using small consortia of species, combining the precision of single-strain probiotics and the holistic approach intrinsic to FMT. The species selection in this oligomicrobial strategy is typically proprietary or based on studies linking single species to disease or health. To advance this approach, we developed the concept of cohesive modules of engraftment (CME) and a workflow for their identification from FMT trials. CMEs represent small donor microbiota subsets that engraft as units (modularity), while maintaining their original composition (cohesiveness). In benchmarking, we identified >200 highly cohesive CMEs (2-5 species) in 5 FMT trials and found evidence for cross feeding as a mechanism for CME integrity. Due to their predictable post-treatment compositions, CMEs deserve investigation as potential ingredients of future therapeutic microbial consortia.},
}

@article {pmid42211393,
year = {2026},
author = {Makranz, C and Huguely, C and Zhang, M and Davis, D and Anderson, B and Haynes, T and Spurgeon, J and Hara, A and Briceno, N and Song, H and Zhang, W and Okada, H and Watanabe, M and Gilbert, MR and Terabe, M},
title = {Inhibition of chemokine CXCL12 modulates the tumor microenvironment in glioblastoma and potentiates immune checkpoint inhibitor efficacy in a tissue-specific manner.},
journal = {Neuro-oncology advances},
volume = {8},
number = {1},
pages = {vdag118},
pmid = {42211393},
issn = {2632-2498},
abstract = {BACKGROUND: Immunotherapy, while effective for many extra-cranial solid tumors, has not shown benefits against glioblastoma. Limited T cell infiltration and an immunosuppressive tumor microenvironment (TME) are among the main barriers to successful immunotherapy. We hypothesized that blocking the chemokine CXCL12 would modulate the TME composition and reverse GBM resistance to immunotherapy.

METHODS: We used a syngeneic murine SB28 GBM model resistant to immune checkpoint inhibitor (ICI) and compared orthotopic and subcutaneous tumors to differentiate tumor-intrinsic factors from CNS-related barriers. We treated SB28 tumor-bearing mice with vehicle, ICI, CXCL12 inhibitor (NOX-A12), or a combination of NOX-A12 with ICI. We assessed treatment effects on immune cell populations in the blood and the TME, and on tumor growth and mouse survival.

RESULTS: ICI alone increased effector CD8[+]T cells in subcutaneous tumors but did not alter immune subsets in intracranial tumors. The combination of NOX-A12 and ICI increased effector CD8[+] and CD4[+] T cells in both models. In subcutaneous tumors, combination treatment also reduced MHC-II[low] tumor-associated macrophages (TAM) and slowed tumor growth. However, in orthotopic tumors, TAM populations remained unaffected, and survival was not extended, despite similar T-cell modulation, supporting the role of TAM in mediating GBM resistance to ICI.

CONCLUSION: CXCL12 inhibition demonstrates therapeutic potential in facilitating anti-tumor immune response by dual mechanism, including T cell expansion and TAM reduction. The inability to deplete TAMs and improve survival in intracranial GBM underscores the need to address brain-specific mechanisms underlying TAM persistence to advance immunotherapy in GBM.},
}

@article {pmid42213435,
year = {2026},
author = {Bhatt, NS and Wang, F and Izumi, S and Chen, Y and Ohlsen, TJD and Armstrong, GT and Huang, IC and Kirchhoff, A and Park, ER and Snyder, C and Yabroff, KR and Yasui, Y and Nathan, PC},
title = {Financial Hardship and Nonadherence to Lifestyle and Surveillance in Childhood Cancer Survivors.},
journal = {JAMA network open},
volume = {9},
number = {5},
pages = {e2615527},
pmid = {42213435},
issn = {2574-3805},
mesh = {Humans ; Female ; *Cancer Survivors/psychology/statistics & numerical data ; Male ; Retrospective Studies ; Adult ; Child ; Young Adult ; *Patient Compliance/statistics & numerical data/psychology ; *Neoplasms ; *Financial Stress/psychology/epidemiology ; Child, Preschool ; Adolescent ; *Healthy Lifestyle ; Life Style ; },
abstract = {IMPORTANCE: The association between medical financial hardship and nonadherence to healthy lifestyle and late-effects surveillance recommendations in long-term survivors of childhood cancer is unknown.

OBJECTIVE: To study the associations between medical financial hardship and nonadherence to healthy lifestyle and late-effects surveillance recommendations.

This retrospective cohort study was performed among participants in the multiinstitutional Childhood Cancer Survivor Study. Participants were 5-year cancer survivors diagnosed at age 21 years or younger between January 1, 1970, and December 31, 1999, and who completed both a medical financial hardship survey between 2017 and 2019 and a follow-up survey assessing lifestyle behaviors and adherence to risk-based surveillance between 2020 and 2022. Data were analyzed between September 29, 2023, and September 2, 2025.

EXPOSURE: Self-reported medical financial hardship determined by an affirmative response to at least 1 item in the material, behavioral, or psychological domains.

MAIN OUTCOMES AND MEASURES: Associations of non-guideline-concordant physical activity, problematic drinking, smoking, and abnormal body mass index with domains of medical hardship were examined using separate multivariable logistic regression models. Associations between a composite lifestyle score (unhealthy, moderately healthy, and healthy) and nonadherence to surveillance for cardiomyopathy or breast, colorectal, cervical, and/or skin cancer were examined using polytomous logistic regression models.

RESULTS: Among 3322 survivors who completed both surveys (median [range] age, 41 [20-69] years; 1751 female [52.7%]), the presence of material, behavioral, and psychological hardship was reported by 1401 (42.2%), 1003 (30.2%), and 1243 (37.4%), respectively. Material hardship was associated with a greater odds of non-guideline-concordant physical activity (odds ratio [OR], 1.67 [95% CI, 1.29-2.18]) and abnormal body mass index (OR, 1.47 [95% CI, 1.15-1.88]). Behavioral and psychological hardships were associated with a higher odds of smoking (OR, 2.29 [95% CI, 1.13-4.62] and 3.95 [95% CI, 2.42-6.44], respectively). Material and psychological hardship were associated with a composite unhealthy lifestyle score (OR, 1.52 [95% CI, 1.11-2.07] and 1.96 [95% CI, 1.31-2.93], respectively), and a higher risk was noted among survivors reporting hardship in at least 2 domains. Psychological hardship was associated with greater nonadherence to skin cancer surveillance (OR, 1.78 [95% CI, 1.05-3.02]) among survivors at high risk due to treatment exposures. Material hardship was associated with greater nonadherence to breast cancer screening (OR, 2.85 [95% CI, 1.27-6.38]) among survivors at average risk. Associations between multiple medical hardship domains and nonadherence to cervical cancer screening were also observed (material and behavioral hardship: OR, 3.20 [95% CI, 1.44-7.14]; material and psychological hardship: OR, 2.18 [95% CI, 1.10-4.35]; behavioral and psychological hardship: OR, 3.25 [95% CI, 1.50-7.04]).

CONCLUSIONS AND RELEVANCE: This cohort study of adult survivors of childhood cancer found that medical financial hardship was associated with nonadherence to healthy lifestyle behaviors and certain recommended surveillance tests for subsequent malignant neoplasms. These findings underscore the need to identify and address medical financial hardship as a potential risk factor of nonadherence to healthy lifestyle and guideline-concordant survivorship care.},
}

Humans
Female
*Cancer Survivors/psychology/statistics & numerical data
Male
Retrospective Studies
Adult
Child
Young Adult
*Patient Compliance/statistics & numerical data/psychology
*Neoplasms
*Financial Stress/psychology/epidemiology
Child, Preschool
Adolescent
*Healthy Lifestyle
Life Style

@article {pmid42204244,
year = {2026},
author = {Lin, HY and Sarkar, I and Mazumder, H and Huang, PY and Muir, KR and Schleutker, J and Pashayan, N and Batra, J and Neal, DE and Grönberg, H and Nielsen, SF and Nordestgaard, BG and Tangen, CM and MacInnis, RJ and Wolk, A and Albanes, D and Travis, RC and Stanford, JL and Mucci, LA and Kibel, AS and Cussenot, O and Berndt, SI and Koutros, S and Sørensen, KD and Cybulski, C and Grindedal, EM and Hoegel, J and Maier, C and Hamilton, RJ and Rosenstein, BS and Vega, A and Kogevinas, M and Wiklund, F and Penney, KL and Teixeira, MR and Brenner, H and John, EM and Kaneva, R and Logothetis, CJ and Neuhausen, SL and De Ruyck, K and Ost, P and Gamulin, M and Usmani, N and Claessens, F and Castelao, JE and Townsend, PA and , and , and Kote-Jarai, Z and Haiman, CA and Eeles, RA and , and Park, JY},
title = {Polygenic risk score with KLK3 SNP-SNP interaction pairs for predicting prostate cancer aggressiveness.},
journal = {Communications medicine},
volume = {},
number = {},
pages = {},
doi = {10.1038/s43856-026-01645-z},
pmid = {42204244},
issn = {2730-664X},
support = {HT9425-23-1-0438//U.S. Department of Defense (United States Department of Defense)/ ; },
abstract = {BACKGROUND: Prostate cancer (PCa) is heterogeneous, making risk stratification essential for clinical care. Although polygenic risk scores (PRSs) with main effects of single-nucleotide polymorphisms (SNPs) can help identify individuals at high risk before biological and clinical onset, a PRS for predicting PCa aggressiveness remains underdeveloped. The KLK3, which encodes prostate-specific antigen (PSA), is linked to PCa aggressiveness. Recent findings on KLK3 SNP-SNP interactions show promise for predicting PCa aggressiveness. The objective of this study is to develop a PRS (PRS-KLK3int) by examining KLK3 SNP-SNP interaction pairs.

METHODS: The PRS-KLK3int was developed based on a discovery set (10,836 PCa patients) and two validation sets with 14,348 and 16,584 patients of European ancestry. A total of 3145 SNP pairs and two published PRSs were evaluated.

RESULTS: This study developed a PRS-KLK3int with 284 SNPs, combining an existing PRS with 270 SNPs and 12 SNP-SNP interaction pairs with 15 SNPs (one overlapped). All these 12 pairs were involved with at least one SNP from KLK3. The PRS-KLK3int outperformed two existing PRSs in predicting PCa aggressiveness (p-values: 3.5×10[-18], 9×10[-14], and 1.7×10[-20] for the three sets). It effectively distinguished high-risk from low-risk groups across all datasets. The top 1% high-risk group had a higher prevalence of PCa aggressiveness than the middle 50% group (45.5% vs. 25.9%, OR = 2.38, p = 2.2×10[-5]) in the discovery set, and similar results were observed in validation sets (OR = 2.56, p = 4.3×10[-6]; OR = 2.07, p = 2.1×10[-5]).

CONCLUSIONS: These findings support PRS-KLK3int as a valuable tool for PCa severity stratification, especially in identifying extremely high-risk PCa patients.},
}

@article {pmid42205853,
year = {2026},
author = {McGee, LA and Rohit, A and Buras, M and Bajaj, G and Chang, JH and Kalman, NS and Grover, R and Akthar, A and Kole, AJ and McDonald, M and Katz, S and Lee, N and Tsai, H and Urbanic, J and Vargas, C and Zeng, J and Molitoris, J and Lester, S and Mohammadi, H and Holtzman, A},
title = {Proton Therapy for Head and Neck Adenoid Cystic Carcinoma: A Multi-institutional Review.},
journal = {International journal of particle therapy},
volume = {20},
number = {},
pages = {101320},
pmid = {42205853},
issn = {2331-5180},
abstract = {PURPOSE: To evaluate efficacy and toxicity (CTCAE v4.0) outcomes in patients with adenoid cystic carcinoma (ACC) treated with proton beam therapy (PBT).

PATIENTS AND METHODS: From 2012 through 2023, 79 patients with non-metastatic ACC were treated with PBT and enrolled on the Proton Collaborative Group (PCG) registry. Kaplan-Meier analyses quantified locoregional control (LRC), disease-free survival (DFS), and overall survival (OS). ACC patients receiving reirradiation with PBT were excluded from this analysis.

RESULTS: Median follow-up was 3 years (0.01-6.72). Twenty-six patients were unable to undergo surgery and received definitive PBT versus postoperative PBT (n=53). Median postoperative PBT dose was 66 GyE and 70 GyE for definitive patients treated with conventional fractionation. Most patients had localized disease (n=75); few had nodal metastases (n=4). 62% were locally advanced (T3-T4) at the time of PBT treatment. 3-year Locoregional control (LRC) for all patients was 98% [95% CI (94.3, 100)]. Advanced T-staging, positive margins and definitive-intent PBT were not associated with worsened LRC. 3-year Progression free survival (PFS) was 80.5% (70.6, 91.7). Patients receiving definitive intent PBT had lower but nonsignificant PFS (73.3% vs. 83.8%, p-0.075). Advanced T-staging and positive margins did not have worsened PFS. Overall survival at 3 years was 89.2% (81.4, 97.8). Acute grade 3 toxicities occurred in 16 patients, the most common included the following: mucositis (n=5), oral pain (n=3), and dermatitis (n=5). Late grade 3 toxicity (n=2) included middle ear inflammation (n=1) and skin ulceration (n=1). There were no grade 4+ toxicities.

CONCLUSION: PBT appears to be highly efficacious in providing LRC for patients with ACC including those patients treated with definitive intent. PBT toxicity was acceptable. Longer follow-up is needed.},
}

@article {pmid42206435,
year = {2026},
author = {Tettero, JM and Zhang, MJ and Liu, W and Nawas, MT and Milano, F and Bejanyan, N and Bachanova, V and Broglie, L and Saber, W and Gui, G and Dillon, LW and Walter, RB and Page, KM and Hourigan, CS and El Chaer, F},
title = {Real-world heterogeneity in the prognostic value of pre-transplant flow cytometry measurable residual disease in acute myeloid leukemia in first complete remission: CIBMTR analysis.},
journal = {Haematologica},
volume = {},
number = {},
pages = {},
doi = {10.3324/haematol.2026.300764},
pmid = {42206435},
issn = {1592-8721},
abstract = {In this real-world, large, observational study from the Center for International Blood and Marrow Transplant Research (CIBMTR), we examined the association between pre-transplant measurable residual disease (MRD) detected by multiparameter flow cytometry (MFC) test results and outcomes after allogeneic hematopoietic cell transplantation (alloHCT) in patients with acute myeloid leukemia (AML) in first complete remission (CR1). We included 2,544 patients who underwent transplant during 2013-2019; 11% had detectable MRD prior to alloHCT. Patients' median age was 58 years. Among MRD-negative and MRD-positive groups, 48% vs 52% received myeloablative conditioning, and 37% vs 29% had matched unrelated donors, respectively. The 1-year cumulative incidence of relapse was 35% in the MRD-positive group and 25% in the MRD-negative group (P < .001). MRD positivity was associated with inferior overall survival (hazard ratio [HR], 1.27; 95% CI, 1.06-1.51; P = .009) and disease-free survival (HR, 1.31; 95% CI, 1.11-1.53; P = .001), and increased relapse risk (HR, 1.42; 95% CI, 1.17-1.72; P < .001), but not with non-relapse mortality. Notably, patients with pre-alloHCT MRD negativity remained at high risk of relapse, underscoring the limited prognostic utility of registryreported MFC-MRD testing due to variability in methods and thresholds. Survival analyses across the 12 largest centers demonstrated substantial variability in the prognostic impact of MRD. These findings underscore that although pre-alloHCT MRD by MFC remains a clinically relevant prognostic biomarker, its reliability is contingent upon methodological standardization across centers. These findings highlight the need for standardized MRD assessment to improve risk stratification in AML.},
}

@article {pmid42207168,
year = {2026},
author = {Zeng, J and Cui, S and Hippe, DS and Fu, J and Yaseen, F and He, Y and Kang, J and Grassberger, C and Vesselle, HJ and Kinahan, PE and Eaton, KD and Baik, CS and Santana-Davila, R and Lee, S and Rengan, R and Bowen, SR},
title = {Mature Outcomes and Patterns of Failure in the Phase II FLARE-RT Trial of Biological Image-guided and Risk-Adaptive Chemoradiation for Unresectable NSCLC.},
journal = {Clinical cancer research : an official journal of the American Association for Cancer Research},
volume = {},
number = {},
pages = {},
doi = {10.1158/1078-0432.CCR-25-2626},
pmid = {42207168},
issn = {1557-3265},
abstract = {PURPOSE: FLARE-RT tested personalized functional-lung-avoidance and response-adaptive radiotherapy intensification for unresectable non-small cell lung cancer (NSCLC) using FDG-PET/CT and SPECT/CT. We report mature outcomes and failure patterns.

METHODS: 49 patients with AJCCv7 stage IIB-IIIB NSCLC enrolled on FLARE-RT (NCT02773238) from 2016-2021 and initiated chemoradiation. Patients with Week 3 FDG-PET response received 60Gy in 30 fractions. Patients with non-response received concomitant boosts Weeks 4-6 to residual metabolic disease of 74-90Gy total guided by FDG uptake. Overall survival (OS, primary endpoint) and progression free survival (PFS) were estimated via Kaplan-Meier. Locoregional progression (LRP) and distant metastasis (DM) cumulative incidence were estimated via Aalen-Johansen, with death and alternative progression pattern as competing risks. Predictors of treatment failure modes were identified through Fine-Gray regression.

RESULTS: At 52.3 months median follow-up, 1-year and 2-year OS were 81.6% (95%CI:71.5-93.2%) and 54.2% (CI:41.8-70.4%), respectively; 1-year and 2-year PFS were 53.1% (CI:40.9-69.0%) and 40.5% (CI:28.8-57.0%), respectively. Cumulative incidence for 1-year and 2-year LRP was 12.2% (CI:4.9-23.2%) and 18.5% (CI:9.0-30.6%), respectively; 1-year and 2-year DM were 34.7% (CI:21.7-48.1%) and 43.1% (CI:28.9-56.5%), respectively. Higher pre-RT FDG-PET total lesion glycolysis (TLG) correlated with increased LRP (HR=1.87 [CI:1.41-2.49], p<0.001), whereas higher mid-RT TLG correlated with DM (HR=1.52 [CI:1.05-2.21], p=0.03). 25 of 49 patients received durvalumab and exhibited lower 1-year DM (20.0% vs. 54.2%, p=0.04) with equivocal 1-year LRP (20.0% vs. 4.2%, p=0.27).

CONCLUSION: Biological image-guided FLARE-RT achieved durable locoregional control with consistent survival outcomes relative to RTOG0616 (60Gy arm) and RTOG1106 (adaptive arm). This informs biomarker-guided and risk-adaptive therapy for unresectable NSCLC.},
}

@article {pmid42207534,
year = {2026},
author = {Schlam, I and Tolaney, SM and Lin, NU and Parsons, H and Morganti, S},
title = {Circulating Tumor DNA in Early Breast Cancer: A Review.},
journal = {JAMA oncology},
volume = {},
number = {},
pages = {},
doi = {10.1001/jamaoncol.2026.1465},
pmid = {42207534},
issn = {2374-2445},
abstract = {IMPORTANCE: Circulating tumor DNA (ctDNA) has emerged as a noninvasive biomarker with the potential to detect minimal residual disease (MRD), monitor treatment response, and identify recurrence (eg, molecular relapse) earlier than conventional clinical or imaging approaches. Although ctDNA-based MRD assays have demonstrated prognostic value in early breast cancer, their optimal clinical utility remains uncertain.

OBSERVATIONS: This review summarizes the current data on ctDNA MRD assays in early breast cancer. Although these assays have established analytical and clinical validity, their clinical utility remains uncertain. Dynamics of ctDNA during neoadjuvant therapy are associated with pathologic complete response and long-term outcomes. Following completion of curative-intent therapy, ctDNA positivity (eg, presence of MRD) is strongly associated with future distant recurrence. Similarly, the emergence of ctDNA during surveillance precedes the clinical diagnosis of overt metastatic disease. Although observational studies and meta-analyses have supported ctDNA as a complementary biomarker for established risk-stratification tools, evidence that demonstrates improved outcomes with ctDNA-guided management remains limited. Furthermore, the optimal timing and frequency of testing remain unknown, and studies comparing assays are lacking. Multiple ongoing prospective interventional trials are evaluating whether ctDNA-guided treatment escalation or de-escalation can improve patient outcomes and support the routine implementation of ctDNA assays in clinical practice.

CONCLUSIONS AND RELEVANCE: ctDNA-based MRD assays hold promise for refining risk stratification, enabling earlier detection of recurrence, and informing treatment decisions in patients with early breast cancer, but clinical utility has not yet been demonstrated. Prospective trials are essential to determine whether ctDNA-guided interventions improve outcomes beyond standard management. Clinicians should understand the strengths, limitations, and evolving evidence base of ctDNA assays, as well as patient preferences, prior to incorporating them into patient care.},
}

@article {pmid42207938,
year = {2026},
author = {Bear Don't Walk Iv, OJ and Yowelunh McLester-Davis, LW and Pete, D and Peter, D and Hernandez-Hernandez, K and Calac, AJ and de la Sierra, VQ and Dhein, K and Henare, K and Tsosie, KS},
title = {Reclaiming Data, Restoring Health: The Indigenous Biomedical Data Science Renaissance.},
journal = {Annual review of biomedical data science},
volume = {},
number = {},
pages = {},
doi = {10.1146/annurev-biodatasci-092524-121351},
pmid = {42207938},
issn = {2574-3414},
abstract = {Indigenous Peoples are leading a renaissance in biomedical data science. Throughout this narrative review, we highlight advancements from leaders in this renaissance across four phases of biomedical data science: ethics and values that inform research, data harmonization, model development and assessment, and commercialization. In addition, we synthesize five teachings that advance biomedical data science: Indigenous sovereignty, ethical stewardship, relationality and trust, community prioritization, and Indigenous worldviews. We conclude with considerations for all biomedical data scientists, Indigenous People in biomedical data science, and Indigenous leaders leveraging biomedical data science to advance Indigenous health and well-being. This renaissance offers a road map for global biomedical systems to evolve beyond colonial legacies toward practices that uphold self-determination, restore balance, embody relationality, and promote the well-being of human and nonhuman kin.},
}

@article {pmid42209122,
year = {2026},
author = {Osborne, D and Cutler, CS and Chaple, IF and Ribeiro Pereira, PM and Peterson, TE and Solingapuram Sai, KK and Wang, J and Scott, PJH and Chen, DL},
title = {Industry-Academic Collaboration in Nuclear Medicine: Proceedings from the 2024 CMIIT Industry Partners Circle.},
journal = {Journal of nuclear medicine : official publication, Society of Nuclear Medicine},
volume = {},
number = {},
pages = {},
doi = {10.2967/jnumed.126.272619},
pmid = {42209122},
issn = {1535-5667},
abstract = {Advancing and streamlining the development pipeline and translation of theranostic radiopharmaceuticals for application in nuclear medicine necessitates continued cross-sector collaboration among key stakeholders from the Society of Nuclear Medicine and Molecular Imaging (SNMMI), industry partners, and academics to ensure continued growth and innovation and clinical translation. One mechanism the SNMMI has for such dialogue is its biennial Industry Partners Circle (IPC). After the success of prior IPCs, the Center for Molecular Imaging, Innovation, and Translation (CMIIT) hosted the latest IPC in January 2024. The goals of the 2024 CMIIT IPC were to address 4 key priorities that have emerged for the translational community: grow the workforce pipeline, improve academia/industry collaborations to support career development, facilitate radiopharmaceutical clinical trials, and overcome barriers in developing α-therapies. The IPC was attended by SNMMI staff and leadership, members of the CMIIT board of directors, key stakeholders from academia, and industry representatives from a broad range of biopharmaceutical companies and equipment manufacturers. This article summarizes the discussions that were conveyed at the 2024 CMIIT IPC.},
}

@article {pmid42201779,
year = {2026},
author = {Banda, K and Davies, HR and Kumar, Y and Memari, Y and Degasperi, A and Radke, M and Rodriguez, I and Gooley, TA and Katz, R and Menghi, F and Harding, T and Lin, K and Liu, ET and Nik-Zainal, S and Swisher, EM},
title = {HRDetect in Tubo-ovarian Carcinoma: Stratification and Therapeutic Implications.},
journal = {Clinical cancer research : an official journal of the American Association for Cancer Research},
volume = {},
number = {},
pages = {},
doi = {10.1158/1078-0432.CCR-25-1629},
pmid = {42201779},
issn = {1557-3265},
abstract = {PURPOSE: To evaluate HRDetect, a mutational-signature-based algorithm, for prognostic utility in tubo-ovarian carcinoma (OC), and to determine if whole-genome sequencing (WGS) with rearrangement signature (RS) analysis can refine genomic classification beyond the traditional homologous recombination deficient (HRD) versus proficient (HRP) framework.

EXPERIMENTAL DESIGN: WGS was performed on matched tumor-normal pairs from 185 patients with advanced-stage OC from the University of Washington (UW) cohort. HRDetect scores were calculated using substitution signatures, rearrangement signatures, microhomology-mediated deletions, and global loss of heterozygosity. An independent validation cohort (ARIEL2, n = 77) of platinum-sensitive OC treated with rucaparib, was analyzed to correlate HRDetect with PARP inhibitor (PARPi) response. RS analysis and unsupervised hierarchical clustering were employed to delineate genomic subgroups.

RESULTS: In the UW cohort, 51.4% of cases were classified as HRDetect-high and had significantly prolonged median overall survival versus others (6.2 vs 4.1 years; HR=0.6; 95% CI=0.41-0.87; p=0.007). 48.4% of HRDetect-high tumors harbored BRCA1/2 mutations or BRCA1 promoter methylation, while 22.1% lacked BRCA1/2 alterations. A substantial fraction (23.2%) fell into an HRDetect-intermediate category, highlighting greater genomic heterogeneity than currently appreciated. RS profiling uncovered eleven genomic clusters, with specific RS profiles (RS1, RS14, RS18) correlating with poor survival. In ARIEL2, HRDetect-high tumors showed better PARPi responses, with improved progression-free survival (11.1 vs 7.1 months; HR=0.44; 95% CI=0.26-0.74; p=0.03) and response rates (54% vs 22.5%).

CONCLUSIONS: HRDetect predicts survival and sensitivity to PARPi in OC. Combined with RS-based clustering, it reveals unappreciated genomic heterogeneity, and supports a nuanced stratification framework to improve precision oncology in OC.},
}

@article {pmid42203177,
year = {2026},
author = {Olbrich, P and Fischer, M and Deyà-Martinez, A and Campos-Asensio, C and Neth, O and Hadjadj, J and Forbes Satter, LR and Leiding, JW and Torgerson, TR and Bakhtiar, S and Baris, S and Badolato, R and Bloomfield, M and Buddingh, EP and Burroughs, LM and Burns, S and Cooper, MA and Crickx, E and Ehl, S and Farmand, S and Freeman, AF and Gonzalez-Granado, LI and Hagin, D and Hanitsch, LG and Hanzlikova, J and Hauck, F and Ivorra-Cortés, J and Körholz, J and Lankester, AC and Leahy, TR and Meyts, I and Milner, JD and Nademi, Z and Pachlopnik Schmid, J and Pergent, M and Prévot, J and Rivière, JG and Roxo-Junior, P and Schuetz, C and Slatter, MA and Soler Palacín, P and Warnatz, K and Vítovcová, P and Vastert, SJ and Neven, B and Albert, MH and Speckmann, C and , },
title = {Guidance on JAK inhibitor treatment for inborn errors of JAK-STAT signaling (2026). An international consensus statement on behalf of the ESID/EBMT-IEWP and ERN-RITA.},
journal = {The Journal of allergy and clinical immunology},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.jaci.2026.05.005},
pmid = {42203177},
issn = {1097-6825},
abstract = {BACKGROUND: Inborn errors of immunity (IEI) associated with gain-of-function (GOF) in the Janus kinase (JAK)/Signal Transducer and Activator of Transcription (STAT) pathways (JAK-STAT GOF IEI) are rare disorders characterized by immune dysregulation, autoimmunity, malignancy and increased infection susceptibility. To date, no JAK inhibitors (JAKi) are licensed for these conditions, but they are frequently prescribed off-label, even though high-quality evidence and treatment guidelines remain limited.

OBJECTIVE: To develop evidence- and consensus-based recommendations for JAKi treatment in JAK-STAT GOF IEI across all age groups based on a systematic literature review and expert consensus.

METHODS: An international expert group conducted a systematic literature review and developed recommendations on JAKi treatment in JAK-STAT GOF IEI using a modified Delphi approach. Recommendations were developed based on published evidence, data from an international retrospective cohort study, and patient representative input. These statements were then tested for consensus in a two round Delphi survey procedure in a larger, interdisciplinary expert panel.

RESULTS: Consensus- and evidence-based guidance is presented across five thematic areas: (I) JAKi indications/contraindications, (II) pre-treatment assessment, (III) pharmacology/dosing, (IV) monitoring, and (V) use in the context of hematopoietic stem cell transplantation. A total of 51 statements were established and contextualized with the available evidence.

CONCLUSION: This consensus provides structured guidance for clinicians managing JAK-STAT GOF IEI with JAKi. While prospective trials will further refine these strategies, this guidance represents the current international standard of care, reflecting the synthesis of clinical experience and the best available evidence.},
}

@article {pmid42203568,
year = {2026},
author = {Maitra, A and Chari, ST and Wu, B and Van Den Eeden, SK and Fisher, W and Vege, SS and Rinaudo, JA and Feng, Z and , },
title = {Towards early detection of pancreatic cancer: The current status of cohort studies by the Diabetes-Pancreatic Ductal AdenoCarcinoma Working Group.},
journal = {Pancreatology : official journal of the International Association of Pancreatology (IAP) ... [et al.]},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.pan.2026.04.020},
pmid = {42203568},
issn = {1424-3911},
abstract = {The Diabetes-Pancreatic Ductal Adenocarcinoma Working Group (DM-PDAC WG) was formed within the Consortium for Study of Chronic Pancreatitis Diabetes and Pancreatic Cancer (CPDPC) to study the link between new-onset diabetes and pancreatic cancer. Its goals were to i) estimate the risk of PDAC in a prospectively assembled cohort of individuals with NOD identified at its glycemic onset (GNOD), ii) Establish a biobank of clinically annotated bio-specimens from GNOD subjects with pre-symptomatic PDAC and control new-onset type 2 DM, iii) Conduct Phase 3 validation studies of promising biomarkers for identification of occult PDAC in GNOD; iv) Provide a platform for development of a future interventional screening protocol for early detection of PDAC in NOD patients that incorporates imaging studies and clinical algorithms. The study identified >20,000 subjects with GNOD and assembled a biobank of serial blood samples in 2270 GNOD subjects. The risk of PDAC in GNOD and the distribution of lead time from GNOD to PDAC clinical diagnosis have been definitively defined in a cohort of 18,838 GNOD subjects identified during the course of the study. Ongoing biomarker and metabolomics studies will not only provide data on performance of tested biomarkers, but also an unprecedented repository of data on a large number of type 2 DM subjects. There are also ongoing studies on the "science of NOD" to understand its pathogenesis. Overall, the DM-PDAC Working Group has been successful in its mission to further our understanding of the link between diabetes pancreatic cancer.},
}

@article {pmid42203843,
year = {2026},
author = {Antwi, SO and Coombes, BJ and Carlson, EE and Larson, NB and Rabe, KG and Atkinson, HJ and Majumder, S and Bamlet, WR and Schaid, DJ and Zhong, J and McKean, D and Arslan, AA and Beane Freeman, LE and Bracci, PM and Canzian, F and Truong, T and Atkins, J and Du, M and Gallinger, S and Goodman, PJ and Katzke, V and Campa, D and Kooperberg, C and Le Marchand, L and Neale, RE and Patel, AV and Wactawski-Wende, J and Perdomo, S and Shu, XO and Visvanathan, K and Van Den Eeden, SK and White, E and Zheng, W and Albanes, D and Andreotti, G and Brennan, P and Chanock, SJ and Chen, Y and Darst, B and Ferrari, P and Giovannucci, EL and Goggins, M and Haiman, C and Hassan, M and Hung, RJ and Jones, MR and Kraft, P and Malats, N and Moore, SC and Ng, K and Peters, U and Porta, M and Rothman, N and Sánchez, MJ and Sesso, HD and Silverman, DT and Southey, MC and Milne, RL and Um, CY and Yu, H and Yuan, C and , and , and Risch, HA and Wolpin, BM and Stolzenberg-Solomon, RZ and Klein, AP and Amundadottir, LT and Oberg, AL},
title = {Polygenic scores for risk of pancreatic ductal adenocarcinoma: evaluation of novel and published models.},
journal = {NPJ precision oncology},
volume = {},
number = {},
pages = {},
doi = {10.1038/s41698-026-01479-x},
pmid = {42203843},
issn = {2397-768X},
support = {K01CA23787/CA/NCI NIH HHS/United States ; U01CA210138/CA/NCI NIH HHS/United States ; R01CA272668/CA/NCI NIH HHS/United States ; },
abstract = {Polygenic risk scores (PRSs) may enhance risk stratification for pancreatic ductal adenocarcinoma (PDAC), but existing models vary widely in design, predictive performance, and cross-ancestry transferability. We developed genome-wide PRSs using Bayesian methods (LDpred2 and PRS-CS) and p value thresholding (PRSice-2) and systematically evaluated these alongside 13 published PRSs to identify models with robust predictive performance across ancestries. Using GWAS summary statistics from 7531 cases and 10,631 controls, we derived the PRSs and tested associations in an independent sample of 4508 PDAC cases and 46,189 controls, with adjustment for well-established PDAC risk factors. Among all models, the genome-wide LDpred2-based PRS showed the strongest association with PDAC (OR = 1.57 per standard deviation increase; 95% CI: 1.51-1.62) and significantly improved discrimination beyond established risk factors alone (AUC = 0.74-0.76; p < 0.0001). Importantly, the genome-wide LDpred2 PRS demonstrated consistent associations across African, Admixed American, and European ancestry groups, whereas the best-performing published PRS was associated with PDAC risk only in individuals of European ancestry. These findings support genome-wide PRSs as a promising framework for multi-ancestry risk stratification for PDAC and to inform targeted early detection strategies.},
}

@article {pmid42189191,
year = {2026},
author = {Sayar, E and Richards, HM and Gulati, R and Patel, RA and Hanratty, B and Lee, HJ and Coleman, I and Mustafi, P and Ding, CC and Chen, WS and Quigley, D and Setty, M and Lang, JM and True, LD and Kollath, L and Lin, DW and Luo, J and Lee, JK and Ha, G and Yu, EY and Cheng, HH and Montgomery, B and Corey, E and Morrissey, C and Schweizer, MT and Nelson, PS and Raychaudhuri, R and Haffner, MC},
title = {Integrative Surface Antigen Profiling of KLK2 and STEAP1 in Advanced Prostate Cancer.},
journal = {Molecular cancer research : MCR},
volume = {},
number = {},
pages = {},
doi = {10.1158/1541-7786.MCR-26-0052},
pmid = {42189191},
issn = {1557-3125},
abstract = {KLK2 and STEAP1 are two cell surface targets with relevance for prostate cancer therapy. The objective of this study was to characterize the expression landscape of KLK2 and STEAP1 in metastatic castration-resistant prostate cancer (mCRPC) and to define associated transcriptomic, genomic, and epigenomic features. We analyzed a total of 1095 patient samples from three mCRPC cohorts, including in situ studies of rapid autopsy cases and patient derived xenograft models. We found that KLK2 and STEAP1 expression is strongly enriched in AR-positive tumors and largely absent in neuroendocrine and double-negative phenotypes. Within AR+ tumors, pairwise comparisons revealed co-expression and high combined positivity rates for STEAP1, KLK2, and PSMA, suggesting that co-targeting any two of these antigens increases overall tumor coverage. Analysis of samples from a rapid autopsy cohort, which enabled assessment of intra- and inter-tumoral diversity, showed comparable degrees of expression heterogeneity for KLK2 and STEAP1. Antigen expression correlated positively with AR genomic alterations and serum PSA levels, and negatively with RB1 and PTEN loss. Transcriptomic and epigenome analyses demonstrated distinct mechanisms governing antigen expression: KLK2 showed a strict AR dependence with coordinated AR/FOXA1/HOXB13 binding and enhancer activation, whereas STEAP1 was only partially AR-dependent and additionally regulated by locus-specific DNA methylation changes. Further, KLK2 and STEAP1 expression states were associated with distinct transcriptional programs and immune microenvironmental features. Implications: These findings establish KLK2 and STEAP1 as key prostate adenocarcinoma-lineage antigens and provide critical insights to inform the rational design and clinical development of cell-surface antigen-directed therapies in prostate cancer.},
}

@article {pmid42189487,
year = {2026},
author = {Jeon, JJ and Chun, H and Lee, J and Son, H and Lee, C and Lee, K and Oh, SS and Hwang, S and Hyun, CS and Kim, MH and Cho, E and Lee, S and Shin, JI},
title = {Evaluating the Performance of Artificial Intelligence in Accurately Detecting Skin Cancer: An Umbrella Review of Systematic Reviews and Meta-analyses.},
journal = {American journal of clinical dermatology},
volume = {},
number = {},
pages = {},
pmid = {42189487},
issn = {1179-1888},
abstract = {BACKGROUND: Artificial intelligence technology is being widely developed in dermatology. However, there remains a lack of comprehensive data analyzing the diagnostic performance of artificial intelligence in skin cancer.

OBJECTIVE: We aimed to evaluate the diagnostic accuracy of artificial intelligence in skin cancer detection.

METHODS: MEDLINE, Embase, Cochrane library, Web of Science, and Scopus were searched from database inception to 9 April, 2025. Studies were included if they exclusively assessed the diagnostic accuracy of artificial intelligence for primary cutaneous malignancies. The artificial intelligence performance in skin cancer diagnosis was evaluated using accuracy, area under the curve value, sensitivity, and specificity.

RESULTS: Twenty-eight systematic reviews and meta-analyses were included. Across the studies, reported sensitivity ranged from 83.7 to 94.4% for basal cell carcinoma, 57.0-90.1% for squamous cell carcinoma, and 48-100% for melanoma. Specificity ranged from 77.9 to 96% for basal cell carcinoma, 92.6-98% for squamous cell carcinoma, and 36-100% for melanoma. Area under the curve values extracted from the reviews varied widely, generally ranged from 0.61 to 0.99. Narrative comparisons within the included studies suggested that deep learning models frequently demonstrated diagnostic performance non-inferior or superior to human clinicians, although prospective validation in real-world clinical workflows remains limited.

CONCLUSIONS: Current evidence suggests that artificial intelligence technologies have demonstrated potential for skin cancer diagnosis, but with important limitations. Variability in diagnostic metrics, driven largely by data heterogeneity and differing validation strategies, poses significant challenges. Emerging evidence suggests future research should transition toward multimodal artificial intelligence systems that integrate structured clinical metadata with image analysis. This will require methodological standardization and validation in real-world settings.},
}

@article {pmid42191051,
year = {2026},
author = {Oshiro, CE and Cushing-Haugen, KL and Vecchio, NJD and Alonge, OD and Ghai, NR and Green, BB and Honda, SA and Neslund-Dudas, C and Ritzwoller, DP and Skinner, CS and Tao, M and Vachani, A and Chubak, J and Corley, DA and Haas, JS and Li, CI and Tiro, JA and Rendle, KA},
title = {Body Mass Index and Initiation of Cancer Screening: A Closer Look at Differences by Race, Ethnicity, and Sex in a Multi-Center Population.},
journal = {American journal of preventive medicine},
volume = {},
number = {},
pages = {108434},
doi = {10.1016/j.amepre.2026.108434},
pmid = {42191051},
issn = {1873-2607},
abstract = {INTRODUCTION: Obesity is associated with risk for several screen-detectable cancers, yet cancer screening rates are lower among adults with obesity. It is unclear whether associations between BMI and screening initiation differ by race, ethnicity, or sex.

METHODS: A retrospective cohort study was conducted among adults initiating cervical, colorectal, or lung cancer screening using electronic health record data from 10 US health systems (2010-2020 for the cervical/colorectal cohorts; 2014-2021 for lung). Associations between screening initiation (within 15 months of becoming age-eligible) and BMI categories were analyzed using separate logistic regression models. Effect modification by race/ethnicity and sex was assessed. Data were analyzed from 2023-2025.

RESULTS: Among 23,849 adults eligible for cervical cancer screening, overweight (BMI 25 to <30 kg/m[2]), class 1 obesity (BMI 30 to <35), class 2 obesity (BMI 35 to <40) and class 3 obesity (BMI 40 or greater), patients had lower odds of screening initiation than adults with healthy weight (BMI 18.5 to <25). Similarly, among 561,132 adults eligible for colorectal cancer screening, overweight and class 1 - 3 obesity were associated with lower odds of screening. Race and ethnicity moderated associations between BMI and cervical (p=0.0013) and colorectal screening (p<0.0001), and sex moderated associations for BMI and colorectal screening (p<0.0001). Stratified analysis was not conducted for the lung cohort (49,199) due to smaller sample size.

CONCLUSION: Adults with obesity have lower odds of timely screening initiation. Given the increased risk of cancers in adults with obesity, effective interventions to target suboptimal cancer screening are critically important.},
}

@article {pmid42191663,
year = {2026},
author = {Kharaji, M and Safwat, AA and Cheng, D and Firoozeh, N and Hassan, MHD and Zhu, C and Orouskhani, M and Guo, Y and Medverd, JR and Cross, NM and Mossa-Basha, M},
title = {Artificial Intelligence in Neuroradiology: A Review of FDA-regulated Algorithms.},
journal = {The British journal of radiology},
volume = {},
number = {},
pages = {},
doi = {10.1093/bjr/tqag120},
pmid = {42191663},
issn = {1748-880X},
abstract = {Artificial intelligence (AI) is increasingly integrated into neuroradiology practice, with a growing number of FDA-cleared algorithms now supporting tasks ranging from acute triage to volumetric analysis. This review provides a structured overview of commercially available, FDA-regulated AI tools in neuroradiology, organized by clinical application. These include detection and prioritization of intracranial hemorrhage and large vessel occlusion, aneurysm identification on CTA, automated ASPECTS scoring, and brain tumor segmentation, as well as tools for image enhancement and quantitative analysis in neurodegenerative and demyelinating diseases. For each application, we describe the algorithm's intended function, summarize available performance data, and highlight areas where AI can add clinical value, such as reducing time to diagnosis, improving detection of subtle findings, or standardizing measurements. We also discuss key limitations, including reduced performance outside intended-use parameters and the need for broader validation. As AI tools continue to evolve, understanding their strengths, limitations, and optimal use cases is essential to their safe and effective deployment in neuroradiology.},
}

@article {pmid42196715,
year = {2026},
author = {Nash, SH and Adcock, R and Wang, C and Hebert-DeRouen, MC and Joe, NS and Pete, D and Kratzer, TB and Wiggins, CL and Liu, L and McDowell, BD},
title = {Area-Level Sociodemographic Differences Between Indian Health Service Purchased/Referred and Non-Purchased/Referred Care Delivery Areas.},
journal = {International journal of environmental research and public health},
volume = {23},
number = {5},
pages = {},
doi = {10.3390/ijerph23050622},
pmid = {42196715},
issn = {1660-4601},
support = {1R21MD018641/MD/NIMHD NIH HHS/United States ; P30 CA086862-25S2/CA/NCI NIH HHS/United States ; P30CA118100/CA/NCI NIH HHS/United States ; Contract HHSN261201800014I, Task Order HHSN26100001/CA/NCI NIH HHS/United States ; P30 CA086862/CA/NCI NIH HHS/United States ; NIH K00CA253685/CA/NCI NIH HHS/United States ; },
mesh = {Humans ; *United States Indian Health Service/statistics & numerical data ; *Indians, North American/statistics & numerical data ; *Health Services Accessibility/statistics & numerical data ; Socioeconomic Factors ; Female ; Socioeconomic Disparities in Health ; Alaska Natives/statistics & numerical data ; Sociodemographic Factors ; Adult ; Male ; Middle Aged ; },
abstract = {PURPOSE: Purchased/Referred Care Delivery Area (PRCDA) counties are those where resident American Indian and Alaska Native (AIAN) people are eligible for Indian Health Service care. Due to concerns about racial misclassification, cancer statistics for AIAN people are often restricted to PRCDA counties. Differences in sociodemographic characteristics may exist between PRCDA and non-PRCDA counties, but have not been described; therefore, the potential selection bias associated with the restriction to PRCDA counties remains unknown.

METHODS: We used data from the University of California, San Francisco Health Atlas to explore ecological differences in county-level demographic, socioeconomic, healthcare access, and health outcomes data between PRCDA and non-PRCDA counties (n = 3152 counties). We tested for statistical differences in mean levels of demographics between PRCDA and non-PRCDA counties using Pooled or Welch t-tests.

RESULTS: We observed small, but statistically significant differences between PRCDA and non-PRCDA counties in county-level demographic and socioeconomic characteristics (age, poverty, utility services threat, unemployment, educational attainment, computer access, and median income), neighborhood and environment characteristics (overcrowding, severe mortgage/rent burden), healthcare access and utilization (uninsured, annual checkup, annual dental visit, mammography, binge drinking, smoking, physical inactivity, social isolation), and health outcomes (poor mental health, arthritis, poor self-rated health, high blood pressure, diabetes, high cholesterol, and obesity).

CONCLUSIONS: These results indicate variability in county-level measures between PRCDA and non-PRCDA counties. While these data do not speak specifically to AIAN peoples' experiences, they provide critical contextual information to understand how exclusion of AIAN people residing in non-PRCDA counties from cancer statistics may bias risk estimates.},
}

Humans
*United States Indian Health Service/statistics & numerical data
*Indians, North American/statistics & numerical data
*Health Services Accessibility/statistics & numerical data
Socioeconomic Factors
Female
Socioeconomic Disparities in Health
Alaska Natives/statistics & numerical data
Sociodemographic Factors
Adult
Male
Middle Aged

@article {pmid42200639,
year = {2026},
author = {Loes, AN and Tarabi, RAL and Li, SH and Atkinson, RK and Huddleston, J and Kikawa, C and Griffiths, T and Drapeau, EM and Wong, S-S and Cheng, SMS and Leung, NHL and Cobey, S and Cowling, BJ and Bedford, T and Hensley, SE and Bloom, JD},
title = {Strain-specific differences in the response to egg-derived versus recombinant protein influenza vaccines.},
journal = {Journal of virology},
volume = {},
number = {},
pages = {e0031726},
doi = {10.1128/jvi.00317-26},
pmid = {42200639},
issn = {1098-5514},
abstract = {UNLABELLED: The 2023/2024 influenza vaccine included an updated H1N1 component designed to better match a new clade of H1N1 that had multiple mutations in antigenic epitopes of hemagglutinin. Despite this update, the vaccine trended toward being less effective against the vaccine-matched H1N1 clade than the parental H1N1 clade lacking the new antigenic mutations. Here, we measure neutralization titers of serum antibodies from individuals who had received either a recombinant protein or an egg-derived vaccine against a set of viruses with hemagglutinins from 58 H1N1 strains representative of the diversity during the 2023/2024 season. We find that egg-derived vaccine recipients, but not recombinant protein vaccine recipients, had a relatively lower boost in neutralizing titers to the new clade that the updated vaccine was designed to target. We suggest that the difference in the extent that the egg-derived vs recombinant protein vaccines boosted neutralizing titers to the new H1N1 clade is because the seed strain for the egg-derived vaccine strain had acquired a reversion of a key antigenic mutation (K142R) present in that clade. Our results show how egg-derived vs recombinant protein vaccines can elicit different relative titer boosts against different subsets of viral strains, a phenomenon that could impact vaccine effectiveness.

IMPORTANCE: Influenza vaccines can be produced from virus grown in eggs or grown in cells or made with recombinant protein. Egg-derived influenza vaccines often contain egg-adaptive mutations in the viral antigen hemagglutinin (HA) which can impact the antigenicity or immunogenicity of the HA. In this study, we compare neutralization titers from egg-derived and recombinant protein vaccine recipients against recently circulating influenza A(H1N1) strains. We find that the egg-derived vaccine induces less of a boost in titers than the recombinant protein vaccine to the new clade of viral strains that the vaccine was designed to target.},
}

@article {pmid42200680,
year = {2026},
author = {Wolf, AMD and Hoffman, RM and Walter, LC and Zeigler-Johnson, C and Church, TR and Guerra, CE and Elkin, EB and Etzioni, R and Herzig, A and Oeffinger, KC and Perkins, RB and Raoof, S and Tina Shih, YC and Skates, SJ and Kratzer, TB and Manassaram-Baptiste, D and Smith, RA},
title = {Colorectal cancer screening: An update to the American Cancer Society guideline, 2026.},
journal = {CA: a cancer journal for clinicians},
volume = {76},
number = {3},
pages = {e70083},
doi = {10.3322/caac.70083},
pmid = {42200680},
issn = {1542-4863},
mesh = {Humans ; *Colorectal Neoplasms/diagnosis/epidemiology ; *Early Detection of Cancer/methods/standards ; United States/epidemiology ; American Cancer Society ; Feces/chemistry ; Middle Aged ; Mass Screening/standards/methods ; Occult Blood ; Aged ; Biomarkers, Tumor ; Practice Guidelines as Topic ; },
abstract = {Colorectal cancer (CRC) is a leading cause of cancer incidence and mortality in the United States, with rates recently increasing among adults younger than 65 years. In 2018, the American Cancer Society (ACS) lowered the recommended age to initiate screening for average-risk adults to age 45 years. Since then, new molecular-based screening tests-a multitarget stool RNA test (mt-sRNA), a next-generation mt-sDNA test, and a blood-based cell-free DNA assay-have received regulatory approval for CRC screening. For this update, the ACS Guideline Development Group commissioned a targeted, systematic evidence review evaluating diagnostic performance and published modeling studies to judge the potential impact of these tests on CRC incidence and mortality. The ACS reaffirms the recommendation that average-risk adults should initiate CRC screening at age 45 years and continue through age 75 years for those with a life expectancy greater than 10 years. Consistent with prior guidelines, the ACS emphasizes that offering multiple, recommended screening options supports informed patient choice and may improve participation, because the most effective screening test is the one that the patient completes. The next-generation mt-sDNA test, which is an updated version of an already recommended mt-sDNA test, and the mt-sRNA test demonstrated high sensitivity for CRC and moderate sensitivity for advanced precancerous lesions and are recommended, along with annual high-sensitivity fecal immunochemical and high-sensitivity guaiac-based fecal occult blood tests, as preferred stool-based screening options at 3-year intervals. Compared with established stool-based tests, blood-based tests demonstrated lower sensitivity for both advanced precancerous lesions and stage I cancers, with modeling studies predicting less effectiveness in reducing CRC incidence and mortality. At this time, blood-based tests should be recommended only to individuals who decline or do not complete preferred screening tests. Ongoing evaluation of adherence, real-world implementation, and clinical outcomes will inform future updates for these new tests. For screening to be effective, a positive result on any noncolonoscopy screening test requires timely follow-up with colonoscopy, preferably within 6 months, to complete the screening process.},
}

Humans
*Colorectal Neoplasms/diagnosis/epidemiology
*Early Detection of Cancer/methods/standards
United States/epidemiology
American Cancer Society
Feces/chemistry
Middle Aged
Mass Screening/standards/methods
Occult Blood
Aged
Biomarkers, Tumor
Practice Guidelines as Topic

@article {pmid42201458,
year = {2026},
author = {Weiss, NS and Kessler, L and Etzioni, R},
title = {The analysis of cancer screening trials in which the outcome is the incidence of late-stage disease.},
journal = {European journal of epidemiology},
volume = {},
number = {},
pages = {},
pmid = {42201458},
issn = {1573-7284},
support = {R35 CA274442/CA/NCI NIH HHS/United States ; },
abstract = {The National Health Service-Galleri randomized trial seeks to determine the extent to which a blood-based multi-cancer screening test can lead to a reduced incidence of a variety of cancers that are at a late stage as of the time of initial diagnosis. In February 2026, the investigators of this trial issued a news release indicating that after several years of follow-up, for a group of 12 pre-specified forms of cancer there was a lower incidence of stage IV cancer among patients in the intervention arm of the trial than in the control arm. The release stated that a group of participants whose stage IV cancer could not have been influenced by the screening - those with stage IV disease already present as of the initial screening exam - had been excluded from this analysis. We argue that while it is appropriate to restrict such an analysis to persons without prevalent stage IV cancer at the start of the trial, a valid result will be obtained only after accounting for the counterparts of these cases that are present in the trial's control arm. We describe how this can be accomplished, and the assumptions needed for such a strategy to succeed.},
}

@article {pmid42185298,
year = {2026},
author = {Mullins, JI and Deng, W and Giorgi, EE and Magaret, CA and Rolland, M and Bhattacharya, T and Westfall, DH and Yssel, AEJ and Bumgarner, RE and Murrell, B and Ndung'u, T and Robb, ML and Rossenkhan, R and Edlefsen, PT and Dong, KL and Chen, L and Gwashu-Nyangiwe, A and Zhao, H and Thebus, R and Ndabambi, N and Galvao, B and Sawe, F and Nitayaphan, S and York, T and Matten, D and Murrell, H and Pankow, AP and Juraska, M and Ludwig, J and Hural, J and Cohen, MS and Corey, L and McElrath, MJ and Gilbert, PB and Williamson, C},
title = {Long-read deep sequencing reveals high rates of multilineage transmission and rapid viral population changes in acute HIV infection.},
journal = {Nature communications},
volume = {},
number = {},
pages = {},
doi = {10.1038/s41467-026-73496-0},
pmid = {42185298},
issn = {2041-1723},
support = {INV-016189/GATES/Gates Foundation/United States ; INV-033558/GATES/Gates Foundation/United States ; UM1 AI068614/AI/NIAID NIH HHS/United States ; UM1 AI068618/AI/NIAID NIH HHS/United States ; P30 AI060354/AI/NIAID NIH HHS/United States ; UKZNRSA1001//International AIDS Vaccine Initiative (International AIDS Vaccine Initiative, Inc.)/ ; 19275//Gilead Sciences (Gilead)/ ; W81XWH-11-2-0174//Henry M. Jackson Foundation (Henry M. Jackson Foundation for the Advancement of Military Medicine)/ ; },
abstract = {Understanding the selective forces acting upon HIV early in infection is crucial to design prevention strategies. By leveraging deep sequencing and the short diagnostic intervals of the FRESH and RV217 cohorts between the last-negative and first-positive RNA tests (median 4 days), we captured a precise and early snapshot of acute HIV infection. The frequency of multiple transmitted viruses of 37% in these as well as placebo recipients from the AMP trials (NCT02716675 and NCT02568215) was higher than previously published, with the true frequency likely to be higher. The relative abundance of lineages fluctuated substantially over time in two-thirds of the multilineage infections, generating uncertainty in identifying the specific viruses that were transmitted and founding the infection. At the population level, viral populations exhibited limited diversity and selection on the Gag and Env proteins at the earliest times examined, with sites inferred to be undergoing negative selection most evident. These data may help explain vaccination failures and provide new targets for prevention.},
}

@article {pmid42185494,
year = {2026},
author = {Xie, Y and Lin, J and Liu, H and Xiong, Y and Han, J and Huang, Z and Weng, J and Wan, Z and Li, P and Wang, P and Liu, X and Wu, L and Cai, Q and Huang, M and Luo, Y and Wang, X and Yu, H},
title = {ICIsAtlas reveals a suppressive NK cell niche in pan-cancer immunotherapy profiles.},
journal = {Communications biology},
volume = {},
number = {},
pages = {},
doi = {10.1038/s42003-026-10336-3},
pmid = {42185494},
issn = {2399-3642},
support = {82272965, 82473456//National Natural Science Foundation of China (National Science Foundation of China)/ ; 82372715//National Natural Science Foundation of China (National Science Foundation of China)/ ; 2025A04J5297//Guangzhou Municipal Science and Technology Project/ ; 2025A04J4447//Guangzhou Municipal Science and Technology Project/ ; 2025A1515011921, 2024A1515030054//Natural Science Foundation of Guangdong Province (Guangdong Natural Science Foundation)/ ; },
abstract = {Immune checkpoint inhibitors (ICIs) have reshaped the treatment in multiple tumors. However, a substantial proportion of patients exhibit limited responses. The lack of harmonized, large-scale pan-cancer ICI datasets coupled with accessible analysis tools hinders the systematic discovery of response biomarkers and resistance mechanisms. Therefore, we developed a comprehensive resource named ICIsAtlas, which encompassed curated transcriptomic and clinical data from 1,268 ICI-treated patients across eight tumor types, with an accompanying R package implementing a complete workflow for deconvolution and biomarker evaluation. Applying the ICIsAtlas framework, a systematic pan-cancer analysis was performed. We identified the universal signatures that were specific for ICI response, including cooperative interactions among favorable immune cells. In addition, we discovered a competitive cell community and SERPING1 + VEGFA+ Natural Killer (NK) cell-mediated immunosuppressive niche in non-responders, which were further validated with single-cell and multiplex immunohistochemistry data. The ICIsAtlas resource and R package represent a powerful, publicly available platform for hypothesis generation and biomarker discovery, which could be used to develop the next-generation biomarkers and therapeutic targets to improve tumor immunotherapy.},
}

@article {pmid42185525,
year = {2026},
author = {Ayoub, HH and Jerome, KR and Chemaitelly, H and Wald, A and Abu-Raddad, LJ},
title = {Mathematical modeling of the population-level impact of hypothetical herpes simplex virus type 2 curative therapy.},
journal = {Communications medicine},
volume = {},
number = {},
pages = {},
doi = {10.1038/s43856-026-01677-5},
pmid = {42185525},
issn = {2730-664X},
abstract = {BACKGROUND: Herpes simplex virus type 2 (HSV-2) infection is a prevalent lifelong infection and the leading cause of genital ulcer disease (GUD), yet no vaccines or curative interventions are currently available. Emerging curative approaches have demonstrated proof-of-concept efficacy in preclinical studies, but their potential population-level impact remains unknown. This study assessed the potential impact of curative therapy on HSV-2 disease burden and transmission.

METHODS: A dynamic HSV-2 transmission model was developed for the United States and calibrated to prevalence estimates from the National Health and Nutrition Examination Surveys. Curative therapy was assumed to be introduced in 2030 and scaled to 20%, 50%, or 80% coverage by 2040 under two scenarios: (i) treatment of symptomatic individuals only and (ii) treatment of all individuals with HSV-2 infection.

RESULTS: Here we show that, by 2050, at 80% coverage, curative therapy for symptomatic individuals reduces the number of 15-49-year-olds with GUD and GUD days by 86.7% and 86.2%, respectively, and decreases the incidence rate and annual new infections by 54.0% and 51.7%, averting 5.4 million cumulative infections. The numbers needed to treat to avert one prevalent or incident symptomatic HSV-2 infection, one incident HSV-2 infection, and one year of GUD days are 0.90, 3.4, and 0.61, respectively.

CONCLUSIONS: Curative therapy could substantially reduce HSV-2 incidence and recurrent GUD, yielding population-level benefits beyond individual cure.},
}