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Hierarchy-Aware Multimodal Unlearning for Medical AI
OpenNovelty: An LLM-powered Agentic System for Verifiable Scholarly Novelty Assessment
OpenNovelty: An LLM-powered Agentic System for Verifiable Scholarly Novelty Assessment
WisPaper: Your AI Scholar Search Engine
Generative AI and Copyright: A Dynamic Perspective
Artificial intelligence in pancreatitis: A narrative review on advancing precision diagnosis, prognosis, and therapeutic strategies
World J Gastroenterol. 2025 Oct 21;31(39):110971. doi: 10.3748/wjg.v31.i39.110971.
ABSTRACT
Pancreatitis poses persistent diagnostic and therapeutic challenges due to its heterogeneous clinical presentation, variable disease course, and lack of targeted interventions. Conventional tools, such as serum enzymes, cross-sectional imaging and clinical scoring systems, often exhibit limited sensitivity and prognostic value, especially during early or atypical stages. Moreover, therapeutic development remains slow, with limited progress toward personalized or mechanism-based strategies. These limitations highlight a critical need for integrative data-driven approaches. Artificial intelligence (AI) has emerged as a promising tool to enhance clinical decision-making in pancreatitis. This narrative review synthesizes recent progress in AI applications across three domains. First, AI-enabled diagnostic platforms incorporating radiomics, deep learning-based imaging analysis, and biomarker optimization have improved early detection and differentiation of pancreatic diseases. Second, AI-driven prognostic models now allow real-time severity prediction, complication forecasting, and recurrence risk assessment, some of which have been deployed in hospital information systems for intensive care units and mortality risk triage. Third, AI-assisted drug discovery and network pharmacology, particularly in combination with traditional Chinese medicine, have revealed novel therapeutic opportunities. Despite encouraging developments, challenges remain in data standardization, model transparency and clinical validation. A multidisciplinary strategy integrating omics data, longitudinal monitoring and pharmacological modeling may help bridge current gaps and advance precision medicine in pancreatitis care.
PMID:41180795 | PMC:PMC12576603 | DOI:10.3748/wjg.v31.i39.110971
Digital twin models for predicting venetoclax and azacitidine-induced neutropenia in patients with acute myeloid leukemia
npj Digital Medicine, Published online: 06 October 2025; doi:10.1038/s41746-025-01978-4
Digital twin models for predicting venetoclax and azacitidine-induced neutropenia in patients with acute myeloid leukemiaAssociation of HTR1F with Prognosis, Tumor Immune Microenvironment, and Drug Sensitivity in Cancer: A Multi-Omics Perspective
Biomedicines. 2025 Sep 11;13(9):2238. doi: 10.3390/biomedicines13092238.
ABSTRACT
Background:HTR1F (5-Hydroxytryptamine Receptor 1F) encodes a G protein-coupled receptor involved in serotonin signaling. Although dysregulated HTR1F expression has been implicated in certain malignancies, its biological functions and clinical significance across cancer types remain largely unexplored. Methods: We performed an integrative pan-cancer analysis of transcriptomic and pharmacogenomic datasets covering 34 cancer types (PAN-CAN cohort, N = 19,131; normal tissues, G = 60,499). Drug sensitivity and molecular docking analyses were conducted using the GSCALite database. The protein-protein interaction (PPI) network of HTR1F was constructed via the STRING database. Additionally, we evaluated the effects of HTR1F overexpression on proliferation and invasion in human lung squamous cell carcinoma (LUSC) cell lines NCI-H520 and NCI-H226. Results:HTR1F expression was significantly upregulated in 17 cancer types and was associated with poor prognosis, with LUSC showing an AUC of 0.912 for 1-year survival prediction. In LUSC, 695 genes were upregulated and 67 downregulated in response to HTR1F overexpression. HTR1F expression correlated with immune-related genes, immune checkpoints, tumor-infiltrating immune cells, tumor mutation burden (TMB), microsatellite instability (MSI), and drug responses. Genomic alterations, including amplification and deletion, were positively associated with HTR1F expression. Drug sensitivity analysis identified compounds such as sotrastaurin (-10.2 kcal/mol), austocystin D (-9.7 kcal/mol), and tivozanib (-9.3 kcal/mol) as potentially effective inhibitors based on predicted binding affinity. Functional enrichment analyses (GO, KEGG) and GSEA revealed that HTR1F is primarily involved in cell cycle regulation, DNA replication, cellular senescence, and immune-related pathways. Functional validation showed that HTR1F overexpression promotes proliferation of LUSC cells via the MAPK signaling pathway. Conclusions: Our integrative analysis highlights HTR1F as a potential biomarker associated with prognosis, immune modulation, and drug sensitivity across multiple cancer types. These findings provide a foundation for future experimental and clinical studies to explore HTR1F-targeted therapies.
PMID:41007799 | PMC:PMC12467612 | DOI:10.3390/biomedicines13092238
Pan-cancer landscape of basement membrane: multi-omics research and single-cell sequencing validation
Cell Cycle. 2025 Aug 13:1-22. doi: 10.1080/15384101.2025.2539645. Online ahead of print.
ABSTRACT
Epithelial carcinoma cells require penetration of the basement membrane (BM) to metastasize. The BM is a thin layer of extracellular matrix beneath epithelial and endothelial tissues. It acts as a structural barrier, preventing cancer cells from invading and undergoing endocytosis and exocytosis. Thus, understanding the relationship between the BM and tumor immunity can lead to new strategies for halting cancer progression and metastasis. Gene expression data of 33 cancers were obtained from the Cancer Genome Atlas database. The study analyzed the correlation between BM regulatory genes, copy number variations, immune-related genes, and tumor immune dysfunction rejection (TIDE). Immunohistochemical methods were used to analyze the expression of regulatory genes. And the BM score was calculated using single-sample gene set enrichment analysis. Single-cell transcriptional sequencing determined the activation status of the BM in the tumor microenvironment. The expression of BM-related genes (BMGs) exhibited significant heterogeneity across different cancer types. Most genes were up-regulated in tumor tissues. Major single nucleotide polymorphisms of BMGs included missense mutations, while major copy number variations were heterozygous deletion and heterozygous amplification. Additionally, the expressions of immune checkpoint molecules CD276, NRP1, and C10orf54 showed positive correlations with BMS. Numerous tumors displayed a significant positive correlation between BMS and TIDE scores. We demonstrate that BM regulatory genes undergo alterations specific to different cancer types, which are associated with the expression of immune checkpoints and immune dysfunction. This indicates that BM remodeling plays an active role in modulating immune resistance, rather than being a passive structural alteration.
PMID:40799172 | DOI:10.1080/15384101.2025.2539645
Integrative spatial analysis reveals tumor heterogeneity and immune colony niche related to clinical outcomes in small cell lung cancer
Cancer Cell. 2025 Feb 14:S1535-6108(25)00030-3. doi: 10.1016/j.ccell.2025.01.012. Online ahead of print.
ABSTRACT
Recent advances have shed light on the molecular heterogeneity of small cell lung cancer (SCLC), yet the spatial organizations and cellular interactions in tumor immune microenvironment remain to be elucidated. Here, we employ co-detection by indexing (CODEX) and multi-omics profiling to delineate the spatial landscape for 165 SCLC patients, generating 267 high-dimensional images encompassing over 9.3 million cells. Integrating CODEX and genomic data reveals a multi-positive tumor cell neighborhood within ASCL1+ (SCLC-A) subtype, characterized by high SLFN11 expression and associated with poor prognosis. We further develop a cell colony detection algorithm (ColonyMap) and reveal a spatially assembled immune niche consisting of antitumoral macrophages, CD8+ T cells and natural killer T cells (MT2) which highly correlates with superior survival and predicts improving immunotherapy response in an independent cohort. This study serves as a valuable resource to study SCLC spatial heterogeneity and offers insights into potential patient stratification and personalized treatments.
PMID:39983726 | DOI:10.1016/j.ccell.2025.01.012
Interplay between gut microbial communities and metabolites modulates pan-cancer immunotherapy responses
Cell Metab. 2025 Jan 28:S1550-4131(24)00495-9. doi: 10.1016/j.cmet.2024.12.013. Online ahead of print.
ABSTRACT
Immune checkpoint blockade (ICB) therapy has revolutionized cancer treatment but remains effective in only a subset of patients. Emerging evidence suggests that the gut microbiome and its metabolites critically influence ICB efficacy. In this study, we performed a multi-omics analysis of fecal microbiomes and metabolomes from 165 patients undergoing anti-programmed cell death protein 1 (PD-1)/programmed death ligand 1 (PD-L1) therapy, identifying microbial and metabolic entities associated with treatment response. Integration of data from four public metagenomic datasets (n = 568) uncovered cross-cohort microbial and metabolic signatures, validated in an independent cohort (n = 138). An integrated predictive model incorporating these features demonstrated robust performance. Notably, we characterized five response-associated enterotypes, each linked to specific bacterial taxa and metabolites. Among these, the metabolite phenylacetylglutamine (PAGln) was negatively correlated with response and shown to attenuate anti-PD-1 efficacy in vivo. This study sheds light on the interplay among the gut microbiome, the gut metabolome, and immunotherapy response, identifying potential biomarkers to improve treatment outcomes.
PMID:39909032 | DOI:10.1016/j.cmet.2024.12.013
Identification of novel germline mutations in <i>FUT7</i> and <i>EXT1</i> linked with hereditary multiple exostoses
Oncogene, Published online: 17 December 2024; doi:10.1038/s41388-024-03254-3
Identification of novel germline mutations in FUT7 and EXT1 linked with hereditary multiple exostoses