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SMILE: A Composite Lexical-Semantic Metric for Question-Answering Evaluation
Artificial Intelligence Index Report 2025
Multimodal analysis of whole slide images in colorectal cancer
npj Digital Medicine, Published online: 24 November 2025; doi:10.1038/s41746-025-02095-y
Multimodal analysis of whole slide images in colorectal cancerTen years of oncogene editorship: a decade of transformation
Oncogene, Published online: 24 November 2025; doi:10.1038/s41388-025-03648-x
Ten years of oncogene editorship: a decade of transformationHealth care Experiences of Educated Young Adults With Blindness in the Digital Age: Qualitative Study
A Biopsy-Free Future: Science Fiction or Science Reality?
JACC Heart Fail. 2025 Nov 21:102782. doi: 10.1016/j.jchf.2025.102782. Online ahead of print.
NO ABSTRACT
PMID:41273317 | DOI:10.1016/j.jchf.2025.102782
Benchmark on Drug Target Interaction Modeling from a Drug Structure Perspective
Reply to: Utilizing foundation models for developing clinical tools
npj Digital Medicine, Published online: 18 November 2025; doi:10.1038/s41746-025-02066-3
Reply to: Utilizing foundation models for developing clinical toolsA Workflow for Full Traceability of AI Decisions
The dual immunomodulatory role of B cells in tumorigenesis: mechanisms, microenvironment crosstalk, and therapeutic implications
Front Immunol. 2025 Oct 30;16:1649812. doi: 10.3389/fimmu.2025.1649812. eCollection 2025.
ABSTRACT
B lymphocytes exhibit a multifaceted and context-dependent role in tumor biology, acting as both promoters and suppressors of malignancy through dynamic interactions within the tumor microenvironment (TME). This review synthesizes current evidence on the dual functions of B cells in tumor immunity, highlighting their capacity to orchestrate antitumor responses via antigen presentation, antibody-dependent cytotoxicity, and tertiary lymphoid structure (TLS)-mediated T cell activation, while paradoxically driving immunosuppression through regulatory B cells (Bregs), pro-angiogenic signaling, and immune checkpoint modulation. Key mechanisms include TLS formation, which enhances cytotoxic T cell priming and correlates with improved immunotherapy outcomes, and Breg-mediated secretion of IL-10/TGF-β, which fosters T cell exhaustion and myeloid-derived suppressor cell recruitment. Tumor-type specificity is evident: TLS-rich malignancies like melanoma and Non-Small Cell Lung Cancer (NSCLC) show B cell-driven immune activation, whereas pancreatic and hepatocellular carcinomas demonstrate B cell functional plasticity influenced by metabolic and epigenetic reprogramming. Therapeutically, B cell-targeted strategies-including CD20 antibodies, CAR-T cells, and B cell epitope vaccines-demonstrate efficacy in hematologic and solid tumors, yet face challenges due to subset heterogeneity and sex-specific response disparities. Emerging approaches combine immune checkpoint inhibitors (ICBs) with TLS-inducing agents or exploit B cell-derived biomarkers for personalized therapy. Future directions emphasize deciphering B cell metabolic-niche crosstalk, optimizing combinatorial regimens, and leveraging spatial multiomics to resolve functional heterogeneity. By bridging mechanistic insights with clinical translation, this work underscores B cells as pivotal regulators of tumor immunity and advocates for precision strategies to harness their antitumor potential while mitigating pro-tumor plasticity.
PMID:41246318 | PMC:PMC12611826 | DOI:10.3389/fimmu.2025.1649812
MedFuse: Multiplicative Embedding Fusion For Irregular Clinical Time Series
LLM4AD: Large Language Models for Autonomous Driving - Concept, Review, Benchmark, Experiments, and Future Trends
Large Language Model Benchmarks in Medical Tasks
Stereo-seq V2: Spatial mapping of total RNA on FFPE sections with high resolution
Targeted inhibition of gastric adenocarcinoma by nano-curcumin liposomes: Insights from combined machine learning and experimental analyses into the mechanisms of cuproptosis and metabolic reprogramming
Int J Pharm. 2025 Nov 9:126368. doi: 10.1016/j.ijpharm.2025.126368. Online ahead of print.
ABSTRACT
PURPOSE: Gastric adenocarcinoma is a highly aggressive malignancy characterized by a complex tumor microenvironment. Nano-curcumin liposomes hold great potential in inhibiting tumor growth and survival, as well as inducing cuproptosis and oxidative stress. Although the anticancer properties of curcumin have been demonstrated, the specific mechanisms by which curcumin inhibites gastric adenocarcinoma through cuproptosis remains unclear. This study investigated how nano-curcumin liposomes mediated the inhibition of gastric adenocarcinoma cell proliferation and survival via cuproptosis.
METHODS: This study utilized the gastric adenocarcinoma cell line AGS to establish 2D and 3D in vitro gastric adenocarcinoma models. Furthermore, we prepared nano-curcumin liposomes to investigate their effects and regulatory mechanisms on AGS gastric adenocarcinoma models. A series of in vitro assays, including flow cytometry, CCK-8, scratch assays and morphological assessments, were performed to evaluate the effects of nano-curcumin liposomes on cell apoptosis, proliferation and migration. Additionally, bioinformatics and machine learning methods were employed to identify key targets that inhibited gastric adenocarcinoma growth and survival associated with nano-curcumin liposomes, which were further validated through RT-qPCR and omics analysis. Computer simulations were also conducted to assess the stability of binding interactions between curcumin and key target proteins.
RESULTS: Cellular experiments demonstrated that nano-curcumin liposomes significantly inhibited proliferation and invasive capacity of gastric adenocarcinoma cells while promoting cellular oxidative stress. Bioinformatics and machine learning analyses identified FDX1, GPX4, SERPINE1 and SLC27A5 as key targets. RT-qPCR results confirmed that nano-curcumin liposomes significantly downregulated the expression of these targets. Molecular dynamics simulations indicated that curcumin could form stable binding interactions with key protein targets.
CONCLUSION: This study revealed that nano-curcumin liposomes inhibited growth and survival of gastric adenocarcinoma cells by interfering with the expression of FDX1, GPX4, SERPINE1 and SLC27A5, which were closely linked to copper-induced oxidative stress. Nano-curcumin liposomes downregulated the expression of FDX1 and GPX4, disrupted mitochondrial energy metabolism, and induced oxidative stress, thereby promoting tumor-associated programmed cell death linked to cuproptosis. Furthermore, by downregulating SERPINE1, nano-curcumin liposomes modulated cell adhesion and migration, inhibiting the invasive and metastatic potential of tumor cells. Finally, downregulation of SLC27A5 altered tumor metabolism and cellular homeostasis, induced oxidative stress, and disrupted intracellular environmental stability, thereby suppressing the growth of gastric adenocarcinoma.
PMID:41218732 | DOI:10.1016/j.ijpharm.2025.126368