Reading view
MedScope: Incentivizing "Think with Videos" for Clinical Reasoning via Coarse-to-Fine Tool Calling
Randomized-controlled trial of skills-based vr vs. distraction vr vs. sham VR for chronic low back pain
npj Digital Medicine, Published online: 16 February 2026; doi:10.1038/s41746-026-02437-4
Randomized-controlled trial of skills-based vr vs. distraction vr vs. sham VR for chronic low back painRare, Yet Targetable: New Perspectives on Ampullary Carcinomas
Int J Mol Sci. 2026 Feb 6;27(3):1597. doi: 10.3390/ijms27031597.
ABSTRACT
Ampullary carcinoma (AC) is a rare gastrointestinal malignancy with dual intestinal and pancreatobiliary differentiation, complicating diagnosis, staging, and treatment. This review synthesizes current epidemiology, pathology, and multi-omic data to outline a pragmatic care pathway: lineage-first at presentation, mutation-fast at progression. Histology remains the primary classifier: the intestinal subtype generally aligns with colorectal regimens, whereas pancreatobiliary and mixed subtypes favor pancreaticobiliary therapy. In selected fit patients, modified FOLFIRINOX may address mixed phenotypes. Next-generation sequencing adds precision by identifying therapeutically relevant alterations, including ERBB2/HER2 amplifications, MSI-high/dMMR, BRAF V600E, and rare NTRK or RET fusions, while KRAS mutations are enriched in pancreatobiliary tumors. We recommend early application of a rapid-core panel (KRAS/BRAF, MSI/dMMR, ERBB2/HER2, RNA-based fusions) to capture high-impact targets, followed by comprehensive profiling at first progression. Liquid biopsy, plasma circulating tumor DNA (ctDNA), or bile-derived DNA may complement tissue and help identify the dominant lineage. Research priorities include ampulla-enriched umbrella trials, explicit AC subcohorts in tissue-agnostic studies, and ctDNA-informed endpoints. This lineage-first, mutation-fast paradigm supports precision care and evidence generation in AC.
PMID:41684016 | PMC:PMC12897727 | DOI:10.3390/ijms27031597
Clinical utility of OGN in pan-cancer: diagnostic biomarker and immune microenvironment regulator
Transl Cancer Res. 2026 Jan 31;15(1):43. doi: 10.21037/tcr-2025-1499. Epub 2026 Jan 27.
ABSTRACT
BACKGROUND: Osteoglycin (OGN), an extracellular matrix protein, has emerging but poorly characterized roles in cancer. This study presents the first pan-cancer investigation of OGN's expression patterns, clinical significance, immune interactions, and functional mechanisms.
METHODS: Multi-omics data from Genotype Tissue Expression (GTEx), Cancer Cell Line Encyclopedia (CCLE), The Cancer Genome Atlas (TCGA), and Human Protein Atlas (HPA) databases were integrated. Differential expression was analyzed in normal tissues and tumor samples. Diagnostic utility was evaluated using area under the curve (AUC) of receiver operating characteristic (ROC) curve. Prognostic value was assessed via Kaplan-Meier [overall survival (OS); disease-specific survival (DSS); disease free interval (DFI); progression-free interval (PFI)] and Cox regression analyses. Immune microenvironment correlations were quantified using ESTIMATE, CIBERSORT, and gene set enrichment. Functional pathways were explored through gene set enrichment analysis (GSEA) and correlation with hallmark cancer signatures.
RESULTS: OGN was broadly expressed in normal tissues (brain, liver, kidney) but significantly downregulated in most tumor types (P<0.05, TCGA; validated at protein level, HPA). OGN demonstrated high diagnostic accuracy in pan-cancer (AUC: 0.703-0.990), achieving near-perfect performance in colon adenocarcinoma (COAD) (AUC: 0.966) and thyroid cancer (THCA) (AUC: 0.920). High OGN expression correlated with improved survival outcomes in thymoma (THYM) (OS/DSS) and cholangiocarcinoma (CHOL) (PFI/DFI), but worse prognosis in lung adenocarcinoma/liver hepatocellular carcinoma (LUAD/LIHC), indicating cancer-type specificity. OGN expression strongly associated with immune cell infiltration (macrophages, natural killer cells, T cells), chemokine signaling, programmed death-ligand 1 (PD-L1) levels, microsatellite instability (MSI), and tumor mutation burden (TMB). GSEA revealed enrichment of OGN-linked genes in epithelial-mesenchymal transition (EMT), angiogenesis, JAK-STAT, and PI3K pathways across cancers.
CONCLUSIONS: Our pan-cancer analysis highlights OGN as a context-dependent regulator linking extracellular matrix (ECM) remodeling with immune and angiogenic signaling. Its pan-cancer dysregulation, diagnostic/prognostic value, and crosstalk with immune evasion mechanisms nominate OGN as a promising multi-functional biomarker and therapeutic target.
PMID:41674945 | PMC:PMC12885879 | DOI:10.21037/tcr-2025-1499
Advancing healthcare AI governance through a comprehensive maturity model based on systematic review
npj Digital Medicine, Published online: 11 February 2026; doi:10.1038/s41746-026-02418-7
Advancing healthcare AI governance through a comprehensive maturity model based on systematic reviewSpatial and multi-omics transcriptomic dissects platinum resistance in lung adenocarcinoma: a five-gene predictive model with tumor microenvironment dynamics
Chem Biol Interact. 2026 Feb 7:111952. doi: 10.1016/j.cbi.2026.111952. Online ahead of print.
ABSTRACT
The scarcity of reliable biomarkers and predictive models for platinum resistance in lung adenocarcinoma (LUAD) poses a significant clinical challenge. This study endeavors to identify molecular subtypes related to platinum resistance and construct a robust predictive model through multi-omics techniques. We performed integrative analysis of public datasets using advanced bioinformatics strategies, including spatial transcriptome deconvolution and consensus clustering. Bulk RNA deconvolution analysis was conducted to characterize tumor microenvironment heterogeneity. Feature selection was performed using the Supervised Principal Component (SuperPC) algorithm, followed by diagnostic model construction validated through receiver operating characteristic (ROC) analysis. Functional validation was performed through cytological experiments measuring cisplatin IC50 alterations following gene manipulation in LUAD cell lines. Consensus clustering revealed distinct LUAD subtypes, with Cluster1 demonstrating significant platinum resistance. We first subtyped the patients in the bulk transcriptome data based on consistency clustering, and then analyzed the differences between different platinum-resistant subtypes (Cluster 1 and Cluster 2), so as to screen 333 isotype-specific differentially expressed genes and 15 platinum resistance-related (PRR) genes were selected through machine learning. A refined 5-gene signature (ANKRD29/CACNA2D2/DSP/HSD17B6/SPP1) achieved exceptional predictive performance (AUC=0.9639). Spatial transcriptomics demonstrated compartmentalized expression patterns: SPP1/DSP localized to tumor niches, HSD17B6/CACNA2D2 to epithelial regions, and ANKRD29 depletion in stromal areas. Cellular colocalization analysis revealed malignant epithelial PH proximity to myeloid and mast cells. Functional validation confirmed that ANKRD29/CACNA2D2 overexpression sensitized A549/DDP cells to cisplatin, while DSP/SPP1/HSD17B6 overexpression induced resistance. Experiments in nude mice have shown that these genes are closely related to cisplatin resistance in LUAD. This study identifies the Cluster1 subtype and malignant epithelial PH as crucial determinants of platinum resistance in LUAD. Our innovative 5-gene predictive model exhibits clinical-grade diagnostic accuracy, and spatial transcriptomic characterization offers mechanistic insights into the dynamics of the tumor microenvironment.
PMID:41662930 | DOI:10.1016/j.cbi.2026.111952
Problems and Barriers Regarding the Admission, Financing, and Service Provision of Digital Health Apps: Qualitative Stakeholder Survey
Call for speakers: TechCrunch Founder Summit 2026
Quantifying Individual Health Status from Multi-omics Data by Health State Manifold
Phenomics. 2025 Dec 15;5(5):469-486. doi: 10.1007/s43657-024-00188-4. eCollection 2025 Oct.
ABSTRACT
Quantifying individual health status from increasingly accumulated omics data is essential for both early prevention and intervention of diseases, which attracts great attention from communities of biology and medicine. Most of the existing approaches mainly classify individuals into different catalogues or classes based on phenotypes and biomarkers. However, an individual's health status from a dynamical systems viewpoint can be viewed as a non-equilibrium steady state, which can generally be characterized by two key features, i.e. (1) homeostatic potential that represents the ability of homeostatic resilience to withstand perturbations or maintain functions at the current state/phenotype of this individual and (2) phenotypic potential that represents the state/phenotype of the individual on the whole process from health to disease. Here, we proposed a health state manifold (HSM) method derived from dynamic network biomarker method and diffusion map theory to quantify individual health status with the characterization of such two features in a robust and accurate manner based on multi-omics data. To verify our method, HSM method was applied to the quantification of diabetes mellitus (rat subjects) and the Roux-en-Y Gastric Bypass (human subjects) for both disease progression process and recovery process, which demonstrated its effectiveness and potential for personalized medicine and preventive medicine.
SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1007/s43657-024-00188-4.
PMID:41659741 | PMC:PMC12881232 | DOI:10.1007/s43657-024-00188-4
Spatial Multi-omics Analyses Reveal Diabetes Promotes Pancreatic Cancer Progression by Stimulating Cholesterol-Induced Neutrophil Extracellular Trap Formation
Cancer Res. 2026 Feb 9. doi: 10.1158/0008-5472.CAN-25-2854. Online ahead of print.
ABSTRACT
Pancreatic ductal adenocarcinoma (PDAC) patients with diabetes mellitus (DM) exhibit poor clinical outcomes. Metabolic reprogramming of both cancer cells and immune compartments plays a crucial role in shaping the anti-tumor immune response in PDAC. DM-induced metabolic alteration may disrupt the intricate crosstalk between immune cells and tumor-associated immune factors, profoundly influencing PDAC progression. Here, we performed an integrated, spatially resolved multi-omics study to investigate DM-associated, cell-specific metabolic remodeling within the PDAC tumor microenvironment. DM influenced interactions between tumor cells and immune cells, which accelerated PDAC growth in both humans and mice. PDAC patients with DM exhibited higher tumor-stage, poorer differentiation, and worse outcomes. Spatial metabolic and transcriptional profiling revealed that SREBP2-dependent cholesterol biosynthesis exacerbated PDAC progression. Increased cholesterol biosynthesis promoted neutrophil recruitment and accelerated formation of neutrophil extracellular traps (NETs) by stimulating the CXCL1-CXCR1/CXCR2 signaling axis, ultimately promoting PDAC growth. Inhibition of SREBP2, pharmacological blockade of CXCL1, or perturbation of NETs markedly reduced PDAC growth in diabetic mouse models. Together, these multi-omics analyses and follow-up mechanistic studies constitute an integrated approach that elucidates a metabolic mechanism by which diabetes promotes PDAC development by remodeling the tumor immune microenvironment and highlights a potential therapeutic strategy for PDAC with DM.
PMID:41661642 | DOI:10.1158/0008-5472.CAN-25-2854
Generating High-quality Privacy-preserving Synthetic Data
Yunjue Agent Tech Report: A Fully Reproducible, Zero-Start In-Situ Self-Evolving Agent System for Open-Ended Tasks
Data-Centric Interpretability for LLM-based Multi-Agent Reinforcement Learning
Exploring AI-Augmented Sensemaking of Patient-Generated Health Data: A Mixed-Method Study with Healthcare Professionals in Cardiac Risk Reduction
Reliability of LLMs as medical assistants for the general public: a randomized preregistered study
Nature Medicine, Published online: 09 February 2026; doi:10.1038/s41591-025-04074-y
In a randomized controlled study involving 1,298 participants from a general sample, performance of humans when assisted by a large language model (LLM) was sensibly inferior to that of the LLM alone when assessing ten medical scenarios leading to disease identification and recommendations for treatment.Sensitive detection of cancer antigens enabled by user-defined peptide libraries
Nature Biotechnology, Published online: 09 February 2026; doi:10.1038/s41587-026-03003-9
Insights into regulatory T cell biology are accelerating therapeutic innovation in cancer immunotherapy, autoimmune diseases and transplant rejection.The Feasibility of Smartwatch Micro–Ecological Momentary Assessment for Tracking Eating Patterns of Malaysian Children and Adolescents in the South-East Asian Community Observatory Child Health Update 2020: Cross-Sectional Study
Cheap AI chatbots transform medical diagnoses in places with limited care
Nature, Published online: 06 February 2026; doi:10.1038/d41586-026-00345-x
Studies in Rwanda and Pakistan reveal real-world utility of chatbots in underfunded clinics, and not just in benchmark tests.