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Multi-Agent Intelligence for Multidisciplinary Decision-Making in Gastrointestinal Oncology
Multi state neurons
Multi-domain performance analysis with scores tailored to user preferences
AI-powered virtual tissues from spatial proteomics for clinical diagnostics and biomedical discovery
Somatic evolution following cancer treatment in normal tissue
Nature, Published online: 10 December 2025; doi:10.1038/s41586-025-09792-4
High-depth sequencing of non-cancerous tissue from patients with metastatic cancer reveals single-base mutational signatures of alcohol, smoking and cancer treatments, and reveals how exogenous factors, including cancer therapies, affect somatic cell evolution.Foundation models in oncology win benchmarks but miss the clinic
Nature Cancer, Published online: 10 December 2025; doi:10.1038/s43018-025-01071-5
Foundation models hold transformative promise for oncology, yet their clinical implementation remains limited, largely owing to their current model design as narrow specialists optimized for static tasks, whereas clinical oncology requires generalist systems capable of integrating multimodal data, capturing disease evolution over time and considering patient perspectives. Design along these requirements is essential to integrating foundation models as trusted partners in cancer care.Pancreatic cancer is evasive. Is the nervous system the reason why?
Nature, Published online: 10 December 2025; doi:10.1038/d41586-025-03943-3
A growing body of research suggests tumours rely on proteins and genes that are unique to the nervous system to persist in the body.Exploring the association between DNA methylation and pancreatic cancer susceptibility through epigenome-wide Mendelian randomization and multi-omics data integration
Epigenetics. 2025 Dec;20(1):2599682. doi: 10.1080/15592294.2025.2599682. Epub 2025 Dec 9.
ABSTRACT
Investigating the role of DNA methylation in the development of pancreatic cancer (PC) may facilitate identification of potential targets for both diagnosis and treatment. We carried out a comprehensive epigenome-wide Mendelian randomization (EWMR) analysis to investigate the correlation of genetically predicted blood CpG sites with PC. Following this, we conducted various sensitivity analyses and repeated analyses using different selection criteria for instrumental variables and conditional Bayesian colocalization to guarantee the reliability of the results. External validation and a meta-analysis were then performed to further validate these results. Next, we conducted CpG site enrichment analysis, overlap with phenome-wide association studies (PheWAS) catalog analysis, overlap with epigenome-wide association studies (EWAS) Toolkit analysis, and drug target analysis to explore the enrichment, biological functions, and potential therapeutic targets associated with these sites. Finally, we used the SMR-IVW software to perform mediation analysis, aiming to uncover potential tumorigenesis pathways of PC at the transcriptional level from three distinct perspectives. Results showed 253 CpG sites passing sensitivity analysis were significantly associated with PC and 159 CpG sites were validated in at least one replication. After meta-analysis, 38 CpG sites were retained, and all 253 CpG sites were classified into three tiers. Among these, cg26373071 (CLPTM1L), cg14271713, cg11652496 (PSTPIP1), and cg20575191 (PSTPIP1) were placed in tier 1 with strong support. Finally, this study identified genetic susceptibility linked to 253 PC-related CpG sites. This study provides insights into the disease's origins and underscores potential targets for future research.
PMID:41368819 | PMC:PMC12694910 | DOI:10.1080/15592294.2025.2599682