HLA-DRA (Major Histocompatibility Complex, Class II, DR Alpha)

Our large-scale GWAS highlights new genetic variants and HLA-linked mechanisms underlying CCA susceptibility. Integrating multi-step post-GWAS approaches enhances understanding of CCA pathogenesis and may facilitate the development of risk biomarkers for early detection and precision prevention strategies.

The data point to hormone-independent proliferative programs and immune-modulating fibroblast subtypes as key contributors. These insights broaden our understanding of tumor biology and may guide the development of targeted, less invasive treatments for young patients.

This study showed that the immune response affects the progress of HER2-BC in a complex mode. These findings greatly improve our understanding of the interaction between immune response and HER2-BC risk, and also help to design therapeutic strategies for HER2-BC from the perspective of immunology.

SNHG26 depletion reversed NK cell suppression and cisplatin resistance in vitro and in vivo. Thus, our study identifies exosomal SNHG26 as a key mediator of cisplatin resistance and NK cell dysfunction in TSCC, suggesting its potential as a promising therapeutic target.

These findings support evaluation of translational strategies, such as CXCR4 inhibition, restoration of antigen presentation, and macrophage reprogramming, to convert "cold" tumors into immune-permissive lesions. Validation in larger, prospective, multicenter cohorts is required.

Tumor-derived MIF is associated with poor prognosis, likely by suppressing the immune system, but it also promotes the induction of APC-like B cells, which are associated with improved outcomes, highlighting its dual role in LUAD. These findings position MIF as a potential therapeutic target and suggest that MIFR+ B cells could serve as important prognostic markers.

By engaging with naive T cells through HLA-DRA via ligand-receptor interactions, CD74⁺ B cells activate transcription factors, including NFKB1, NFKB2, NFATC1, NFATC2, FOS, and RUNX1, in naive T cells, thereby enhancing the immune response. Consequently, CD74⁺ B cells represent a compelling biomarker for and therapeutic target of PSCC, offering profound insights into the immunological mechanisms that drive PSCC progression and response to immunotherapy.

F6: inflammatory myofibroblasts were predicted to recruit neutrophils, monocytes and B cells across multiple human tissues. Our study provides a harmonized nomenclature for skin fibroblasts in health and disease, contextualized with cross-tissue findings and clinical skin disease profiles.

The ICDRS exhibited excellent predictive performance and broad applicability, suggesting it as a powerful tool for prognosis and therapy response. The current study may contribute to more adequate patient selection in the context of tailored therapies.

Molecular docking studies confirmed strong binding affinity of verteporfin (ITGA4 inhibitor, docking score=-16.0 kcal/mol) and ebselen (MPO inhibitor) to their respective targets, suggesting potential therapeutic strategies to overcome chemotherapy resistance. This study establishes a robust 13-gene exosome-based prognostic signature for AML risk stratification and identifies novel immunomodulatory mechanisms mediated by exosome-driven Treg polarization.

These transcriptional features may also reflect greater immunogenicity and inflammation sensitivity. The APC metabolic signature may serve as a useful biomarker to identify GBM subpopulations with reduced stemness and increased immune engagement, offering potential therapeutic implications.

Our results highlight the importance of a combinational strategy employing both epigenetic and immunotherapy in HNSCC.