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Hurdle-RMIL: Addressing Zero Inflation and Long-Tailed Imbalance in Infrared Rainfall Retrieval
GigaBrain-WBC-0.5: A Behavior World Model for Robust Whole-Body Control with Environment Interaction
Lineage-specific pulmonary transcriptome landscape of coronavirus infection unveils universal immunotherapy for viral pneumonia
Efficient Diversity-based Experience Replay for Deep Reinforcement Learning
Targeting peripheral 5-HT2AR enhances antitumor immunity in colorectal cancer
Don't Retrain, Just Reuse: Recovering Dual-Target Molecules from Single-Target Diffusion Models
DeepEN: A Deep Reinforcement Learning Framework for Personalized Enteral Nutrition in Critical Care
Characterization of dysbiosis patterns in gut microbiota of digestive system cancers: an umbrella review
Front Microbiol. 2026 Apr 28;17:1782471. doi: 10.3389/fmicb.2026.1782471. eCollection 2026.
ABSTRACT
Digestive system cancers (DSCs) represent a substantial global health burden. In recent years, the role of gut microbiota in the DSCs has garnered considerable attention, but its change pattern during tumor progression and the specific mechanisms are still not fully understood. We conducted a comprehensive systematic review to characterize patterns of gut microbiota dysbiosis across different DSC types and assess their clinical significance. We systematically searched four English and three Chinese databases up to January 2025 to identify systematic reviews focused on the dynamic characteristics of the gut microbiota during gastrointestinal tumorigenesis. Microbiota biodiversity and taxonomic composition were extracted to identify specific signatures associated with DSCs. The ROBIS tool was used to evaluate the methodological quality of the included studies. Ultimately, 59 studies involving six distinct DSC types were included. Data synthesis and comparison revealed distinct microbiota profiles across DSCs. At the phylum level, Bacillota was decreased in esophageal cancer (EC) and pancreatic ductal adenocarcinoma (PDAC), Pseudomonadota was augmented in EC but exhibited divergent trajectories in colorectal cancer (CRC) and PDAC. Genus-level analyses revealed Veillonella enrichment in EC and PDAC, and Fusobacterium outgrowth in EC, gastric cancer (GC) and CRC. Parvimonas and Streptococcus showed a concordant ascending trend in GC and CRC. Prevotella was overrepresented in EC and GC. This synthesis delineates a qualitative landscape of gut microbiota imbalances associated with various DSCs, highlighting the potential for these microbial shifts to serve as markers for early detection and targeted therapy. Multiomics integration and prospective cohort studies should be prioritized to accelerate clinical translation.
PMID:42131199 | PMC:PMC13161176 | DOI:10.3389/fmicb.2026.1782471
FDX1 as a predictive biomarker and therapeutic target for lymph node metastasis in gastric cancer
Clin Exp Med. 2026 May 10. doi: 10.1007/s10238-026-02160-0. Online ahead of print.
ABSTRACT
The prognostic values of cuproptosis-related genes (CRGs) in gastric cancer with lymph node metastasis (GCLM), especially in the tumor immune microenvironment (TIME), remain unclear. We analyzed the expression, mutation, immunity, drug sensitivity, and prognostic value of CRGs in GCLM using TCGA and GEO cohorts. Consensus clustering was performed to identify CRG subtypes, with differences characterized by multi-omics analysis. A CRG-based prognostic risk score and immune score were constructed for individualized assessment, and the role of CRGs was validated through in vitro and in vivo experiments. Consensus clustering revealed that CRGs were significantly enriched in biological processes related to mitosis and energy metabolism, as well as in immune-related and cancer-associated pathways. Four distinct CRG subtypes were identified, showing marked differences in expression profiles, prognosis, genetic alterations, TIME, and chemotherapeutic drug sensitivity. We developed an exploratory CRG-based prognostic risk score for preliminary individualized assessment, and the functional relevance of CRGs in GCLM was further validated through in vitro experiments. Among these, FDX1, LIAS, DLAT, MTF1, and GLS were identified as key determinants of overall survival in patients with GCLM, with FDX1 emerging as a potential independent prognostic factor. Notably, upregulation of FDX1 significantly suppressed lymph node metastasis of gastric cancer cells in a mouse popliteal lymph node metastasis model. Our data uncovers FDX1 might be a potential favorable prognostic factors in GCLM patients. These findings may improve our understanding of CRGs in GCLM and provide new in-sights for assessing prognosis and developing more effective treatment strategies.
PMID:42107026 | DOI:10.1007/s10238-026-02160-0
Saturation editing of <i>RNU4-2</i> reveals distinct dominant and recessive disorders
Nature, Published online: 08 April 2026; doi:10.1038/s41586-026-10334-9
Saturation genome editing of RNU4-2 identifies the functional and clinical impact of variants across the entire gene and delineates variants that cause a new recessive neurodevelopmental disorder distinct from ReNU syndrome.Stabilizing Rubric Integration Training via Decoupled Advantage Normalization
Rethinking the Role of Entropy in Optimizing Tool-Use Behaviors for Large Language Model Agents
Behavioral Consistency Validation for LLM Agents: An Analysis of Trading-Style Switching through Stock-Market Simulation
Fluid-Derived Organoids from Pleural Effusion and Ascites: Emerging Models for Drug Resistance and Personalized Oncology
J Cancer. 2026 Mar 4;17(3):614-625. doi: 10.7150/jca.127511. eCollection 2026.
ABSTRACT
Malignant pleural effusion (MPE) and malignant ascites (MA) are common complications in advanced-stage cancers, often signifying disease progression and resistance to treatment. Compared to tissue biopsies or surgical specimens, materials derived from effusions offer advantages such as minimal invasiveness, ease of accessibility, and the feasibility of repeated collection during therapeutic interventions. Organoids generated from tumor cells in effusions, termed fluid-derived organoids (FDOs), have demonstrated the ability to maintain genetic heterogeneity and accurately replicate patient-specific tumor phenotypes. These characteristics position FDOs as promising models for investigating drug resistance mechanisms and informing personalized oncology strategies. In the context of lung cancer, organoids derived from pleural effusions have been employed to study acquired resistance to epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors and immunotherapy. Similarly, in ovarian and gastrointestinal cancers, organoids derived from ascites have proven to be valuable platforms for examining chemotherapy resistance and conducting drug sensitivity testing. FDOs have shown significant potential for translational applications by effectively correlating ex vivo drug responses with clinical outcomes, thus facilitating real-time monitoring of resistance evolution. However, several challenges remain, such as achieving culture standardization, maintaining the integrity of tumor microenvironment components, and integrating with multi-omics approaches. This review provides a comprehensive overview of recent advancements in the use of pleural effusion- and ascites-derived organoids for drug resistance research, underscores their applications in personalized oncology, and explores future research directions.
PMID:41869438 | PMC:PMC13003542 | DOI:10.7150/jca.127511
Fluid-Derived Organoids from Pleural Effusion and Ascites: Emerging Models for Drug Resistance and Personalized Oncology
J Cancer. 2026 Mar 4;17(3):614-625. doi: 10.7150/jca.127511. eCollection 2026.
ABSTRACT
Malignant pleural effusion (MPE) and malignant ascites (MA) are common complications in advanced-stage cancers, often signifying disease progression and resistance to treatment. Compared to tissue biopsies or surgical specimens, materials derived from effusions offer advantages such as minimal invasiveness, ease of accessibility, and the feasibility of repeated collection during therapeutic interventions. Organoids generated from tumor cells in effusions, termed fluid-derived organoids (FDOs), have demonstrated the ability to maintain genetic heterogeneity and accurately replicate patient-specific tumor phenotypes. These characteristics position FDOs as promising models for investigating drug resistance mechanisms and informing personalized oncology strategies. In the context of lung cancer, organoids derived from pleural effusions have been employed to study acquired resistance to epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors and immunotherapy. Similarly, in ovarian and gastrointestinal cancers, organoids derived from ascites have proven to be valuable platforms for examining chemotherapy resistance and conducting drug sensitivity testing. FDOs have shown significant potential for translational applications by effectively correlating ex vivo drug responses with clinical outcomes, thus facilitating real-time monitoring of resistance evolution. However, several challenges remain, such as achieving culture standardization, maintaining the integrity of tumor microenvironment components, and integrating with multi-omics approaches. This review provides a comprehensive overview of recent advancements in the use of pleural effusion- and ascites-derived organoids for drug resistance research, underscores their applications in personalized oncology, and explores future research directions.
PMID:41869438 | PMC:PMC13003542 | DOI:10.7150/jca.127511