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cs.AI, q-bio.NC updates on arXiv.org
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TSHA: A Benchmark for Visual Language Models in Trustworthy Safety Hazard Assessment Scenarios
arXiv:2603.29759v1 Announce Type: cross Abstract: Recent advances in vision-language models (VLMs) have accelerated their application to indoor safety hazards assessment. However, existing benchmarks suffer from three fundamental limitations: (1) heavy reliance on synthetic datasets constructed via simulation software, creating a significant domain gap with real-world environments; (2) oversimplified safety tasks with artificial constraints on hazard and scene types, thereby limiting model gene
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cs.AI, q-bio.NC updates on arXiv.org
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Generative AI in Action: Field Experimental Evidence from Alibaba's Customer Service Operations
arXiv:2603.29888v1 Announce Type: cross Abstract: In collaboration with Alibaba, this study leverages a large-scale field experiment to assess the impact of a generative AI assistant on worker performance in e-commerce after-sales service. Human agents providing digital chat support were randomly assigned with access to a gen AI assistant that offered two core functions: diagnosis of customer issues and solution proposals, presented as text messages. Agents retained discretion to adopt, modify,
Generative AI in Action: Field Experimental Evidence from Alibaba's Customer Service Operations
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cs.AI, q-bio.NC updates on arXiv.org
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ContractSkill: Repairable Contract-Based Skills for Multimodal Web Agents
arXiv:2603.20340v2 Announce Type: replace-cross Abstract: Self-generated skills for web agents are often unstable and can even hurt performance relative to direct acting. We argue that the key bottleneck is not only skill generation quality, but the fact that web skills remain implicit and therefore cannot be checked or locally repaired. To address this, we present ContractSkill, a framework that converts a draft skill into an executable artifact with explicit procedural structure, enabling det
ContractSkill: Repairable Contract-Based Skills for Multimodal Web Agents
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(Multiomics OR Omics) AND (Pancreatic)
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Robust transcriptomic hallmarks targeting intratumor heterogeneity in intrahepatic cholangiocarcinoma
Cell Rep Med. 2026 Mar 30:102708. doi: 10.1016/j.xcrm.2026.102708. Online ahead of print.ABSTRACTIntratumor heterogeneity (ITH) undermines transcriptome-based stratification in intrahepatic cholangiocarcinoma (iCCA). Here, we integrate multi-omics data from multi-region, single-region, and single-cell RNA sequencing cohorts to systematically characterize gene expression ITH. We uncover that immune and stromal heterogeneity are primary drivers of ITH, leading to misclassification of a median 27.8
Robust transcriptomic hallmarks targeting intratumor heterogeneity in intrahepatic cholangiocarcinoma
Cell Rep Med. 2026 Mar 30:102708. doi: 10.1016/j.xcrm.2026.102708. Online ahead of print.
ABSTRACT
Intratumor heterogeneity (ITH) undermines transcriptome-based stratification in intrahepatic cholangiocarcinoma (iCCA). Here, we integrate multi-omics data from multi-region, single-region, and single-cell RNA sequencing cohorts to systematically characterize gene expression ITH. We uncover that immune and stromal heterogeneity are primary drivers of ITH, leading to misclassification of a median 27.8% of tumors by existing subtyping systems. To overcome this, we identify a low-intratumor-heterogeneity/high-intertumor-variability (LIHV) gene set and develop an ITH-insensitive classification system defining five subgroups: inflammatory (SI), metabolic (SII), atypical (SIII-1), immune-silent (SIII-2), and neurodegenerative (SIII-3). These subgroups exhibit distinct clinical outcomes, molecular features, immune landscapes, and therapeutic vulnerabilities. GPRC5A and VTCN1 serve as robust immunohistochemical biomarkers for SI and SIII tumors, while serum CEA and CA19-9 identify inflammatory iCCA. Therapeutically, HSP90 inhibition synergizes with anti-PD1 in inflammatory iCCA, whereas combined anti-PD1 and anti-TIM3 suppresses neurodegenerative iCCA. Collectively, our study provides a robust molecular framework and actionable therapeutic strategies for iCCA.
PMID:41916296 | DOI:10.1016/j.xcrm.2026.102708
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Cell Death Discovery nature.com science feeds
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Doxorubicin promotes the production of inflammatory cytokines in tumor-associated macrophages through activating lactate dehydrogenase A
Cell Death Discovery, Published online: 31 March 2026; doi:10.1038/s41420-026-03014-0Doxorubicin promotes the production of inflammatory cytokines in tumor-associated macrophages through activating lactate dehydrogenase A
Doxorubicin promotes the production of inflammatory cytokines in tumor-associated macrophages through activating lactate dehydrogenase A
Cell Death Discovery, Published online: 31 March 2026; doi:10.1038/s41420-026-03014-0
Doxorubicin promotes the production of inflammatory cytokines in tumor-associated macrophages through activating lactate dehydrogenase A-
Omics in Hepatocellular
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Proposed Role of Circadian Clock Genes in Pathogenesis of HCC: Molecular Subtyping and Characterization
Biomedicines. 2026 Mar 12;14(3):645. doi: 10.3390/biomedicines14030645.ABSTRACTBackground: Hepatocellular carcinoma (HCC) stands as a prevalent global health issue with increasing incidence and mortality rates. Hepatocellular carcinoma (HCC) exhibits profound molecular and clinical heterogeneity, which limits the effectiveness of current therapeutic strategies. Circadian rhythm disruption has been implicated in metabolic reprogramming, proliferation, and immune modulation in cancer, but its role
Proposed Role of Circadian Clock Genes in Pathogenesis of HCC: Molecular Subtyping and Characterization
Biomedicines. 2026 Mar 12;14(3):645. doi: 10.3390/biomedicines14030645.
ABSTRACT
Background: Hepatocellular carcinoma (HCC) stands as a prevalent global health issue with increasing incidence and mortality rates. Hepatocellular carcinoma (HCC) exhibits profound molecular and clinical heterogeneity, which limits the effectiveness of current therapeutic strategies. Circadian rhythm disruption has been implicated in metabolic reprogramming, proliferation, and immune modulation in cancer, but its role in shaping HCC heterogeneity remains poorly defined. Methods: Four public HCC transcriptomic cohorts (TCGA-LIHC, CHCC, LIRI, LICA) were integrated using RMA normalization and ComBat for batch correction. Consensus clustering based on 31 core circadian clock genes (CCGs) identified robust molecular subtypes. Multi-omics characterization-including genomic alterations, pathway activity (GSEA/GSVA), immune microenvironment profiling (CIBERSORT, EPIC, MCP-counter, xCell), and drug-sensitivity prediction (pRRophetic/oncoPredict)-was performed to delineate subtype-specific biological properties. A nine-gene CCG-based RiskScore model was constructed using LASSO Cox regression to internally validate subtype robustness and intra-subtype risk stratification. Results: Using consensus clustering of 31 core CCGs in TCGA-LIHC and three independent validation cohorts (CHCC, LIRI, LICA), we identified three reproducible subtypes-Cluster-1 (metabolic-quiescent), Cluster-2 (transition-intermediate), and Cluster-3 (proliferation-inflammatory)-which were recapitulated across cohorts and showed distinct overall survival (Cluster-3 worst; log-rank p values significant across datasets). Multi-omic characterization revealed that Cluster-3 exhibits the highest tumor mutational burden and CNV burden with enrichment of TP53/AXIN1/TERT alterations, strong activation of cell-cycle, E2F, and G2M programs, and an immune-hot yet immunosuppressed microenvironment enriched for TAMs, Tregs and MDSCs. By contrast, Cluster-1 shows relative genomic stability, dominant hepatic metabolic signatures (fatty-acid oxidation, bile-acid and xenobiotic metabolism) and an immune-cold phenotype. Single-cell mapping linked ALAS1 expression to malignant hepatocytes predominating in Cluster-1, whereas NONO and CSNK1D localized to stromal (CAFs/TECs) and both malignant/immune compartments respectively in Cluster-3, providing a cellular mechanism for subtype-specific metabolism, angiogenesis and immune modulation. Finally, a nine-gene CCG-based RiskScore validated prognostic stratification and drug-sensitivity predictions indicated subtype-specific therapeutic vulnerabilities (notably increased predicted TKI sensitivity in Cluster-3). Conclusion: In conclusion, this study proposes a robust circadian rhythm-based molecular classification of hepatocellular carcinoma, revealing three biologically and clinically distinct subtypes characterized by divergent genomic alterations, metabolic programs, immune microenvironment states, and prognostic patterns. By integrating bulk and single-cell transcriptomic data, we identify subtype-specific roles of key circadian regulators-including ALAS1, NONO, and CSNK1D-in shaping tumor metabolism, proliferation, stromal remodeling, and immune suppression. These findings highlight circadian dysregulation as a potential upstream factor associated with HCC heterogeneity and provide a conceptual framework for developing subtype-tailored mechanistic studies and circadian-informed therapeutic strategies.
PMID:41898292 | PMC:PMC13024568 | DOI:10.3390/biomedicines14030645
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Omics in Hepatocellular
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SVNeoPP: A Workflow for Structural-Variant-Derived Neoantigen Prediction and Prioritization Using Multi-Omics Data
Biology (Basel). 2026 Mar 19;15(6):492. doi: 10.3390/biology15060492.ABSTRACTBACKGROUND: Tumor neoantigens are key targets for personalized vaccines and T-cell therapies, yet most pipelines focus on neoantigens derived from SNV/small indel and often yield a limited number of high-quality candidates. SVs are prevalent in tumors and can generate novel chimeric sequences and neopeptides, making them a promising additional source of neoantigens. However, SV-derived neoantigen prediction remains chal
SVNeoPP: A Workflow for Structural-Variant-Derived Neoantigen Prediction and Prioritization Using Multi-Omics Data
Biology (Basel). 2026 Mar 19;15(6):492. doi: 10.3390/biology15060492.
ABSTRACT
BACKGROUND: Tumor neoantigens are key targets for personalized vaccines and T-cell therapies, yet most pipelines focus on neoantigens derived from SNV/small indel and often yield a limited number of high-quality candidates. SVs are prevalent in tumors and can generate novel chimeric sequences and neopeptides, making them a promising additional source of neoantigens. However, SV-derived neoantigen prediction remains challenging due to breakpoint uncertainty, isoform-dependent coding inference, and limited integration of multi-dimensional evidence and reproducibility.
METHODS: We developed SVNeoPP (Structural Variant Neoantigen Prediction and Prioritization), an end-to-end workflow for SV-derived neoantigen analysis. SVNeoPP takes WGS and RNA-seq as inputs, performs SV calling and annotation, and reconstructs altered transcripts and coding sequences in a traceable, isoform-aware manner to generate candidate peptides. Candidates are prescreened by integrating antigen-processing features with HLA binding prediction, and then hierarchically filtered and prioritized based on transcript expression, LC-MS/MS proteomics evidence, immunogenicity predictions, and sequence similarity to experimentally validated neoantigen databases. SVNeoPP is implemented in Snakemake to enable modular extension, checkpoint-based restarts, and end-to-end reproducibility.
RESULTS: Using a hepatocellular carcinoma (HCC) multi-omics dataset as a proof of concept, we demonstrated the performance of SVNeoPP and obtained a high-priority shortlist of candidate peptides. Compared with other methods, SVNeoPP substantially expanded the candidate search space for SV-derived neoantigens and showed more favorable distributions of antigen-processing and HLA binding features.
CONCLUSIONS: SVNeoPP provides a reusable, traceable, and interpretable multi-dimensional evidence-driven framework for SV-derived neoantigens. As a complementary module to SNV/small-indel pipelines, it broadens the neoantigen candidate repertoire and generates ranked candidates with interpretable evidence to facilitate downstream prioritization and decision-making.
PMID:41892252 | PMC:PMC13024079 | DOI:10.3390/biology15060492