Normal view
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Cell
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Sequencing-free whole-genome spatial transcriptomics at single-molecule resolution
(Cell 188, 6953–6970.e1–e8; November 26, 2025)
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cs.AI, q-bio.NC updates on arXiv.org
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Toward Robust Personalized Alignment for LLMs: Mitigating Persona Drift in Multi-Turn Dialogue
arXiv:2609.12373v1 Announce Type: new Abstract: Persona drift remains a central challenge for personalized language models, as user profiles evolve over long interactions rather than remain permanently fixed. Models must therefore revise persistent persona states when preferences genuinely change, while avoiding updates driven by transient, ambiguous, or unresolved observations. We propose CORE, which separates turn-local evidence from persistent persona-state revision and selectively updates g
Toward Robust Personalized Alignment for LLMs: Mitigating Persona Drift in Multi-Turn Dialogue
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cs.AI, q-bio.NC updates on arXiv.org
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Beyond the Query: Do Retrieval Signals Improve Adaptive Multimodal RAG Routing?
arXiv:2609.12437v1 Announce Type: cross Abstract: Adaptive RAG often uses retrieval-time signals to decide whether another retrieval, reranking, or multimodal step should run. We ask whether these signals add routing value once the query itself is already known. Across document, audio, and video RAG, we compare matched query-only and query+retrieval routers while holding the optional actions, router family, training procedure, and evaluation fixed. On the held-out final evaluation, adding the t
Beyond the Query: Do Retrieval Signals Improve Adaptive Multimodal RAG Routing?
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Omics in Hepatocellular
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Key Experimental Therapeutics and Knowledge Gaps in Metabolic Dysfunction-Associated Steatohepatitis (MASH)
Drug Des Devel Ther. 2026 Sep 5;20:543657. doi: 10.2147/DDDT.S543657. eCollection 2026.ABSTRACTMetabolic dysfunction-associated steatohepatitis (MASH) is not solely a disorder of hepatocellular lipid accumulation, but a multicellular disease driven by coordinated metabolic stress, sterile inflammation, fibrogenesis, and niche remodeling. Recent therapeutic progress with the provisional approval of resmetirom and semaglutide has validated MASH as a tractable clinical target. However, many experim
Key Experimental Therapeutics and Knowledge Gaps in Metabolic Dysfunction-Associated Steatohepatitis (MASH)
Drug Des Devel Ther. 2026 Sep 5;20:543657. doi: 10.2147/DDDT.S543657. eCollection 2026.
ABSTRACT
Metabolic dysfunction-associated steatohepatitis (MASH) is not solely a disorder of hepatocellular lipid accumulation, but a multicellular disease driven by coordinated metabolic stress, sterile inflammation, fibrogenesis, and niche remodeling. Recent therapeutic progress with the provisional approval of resmetirom and semaglutide has validated MASH as a tractable clinical target. However, many experimental agents have shown limited or inconsistent efficacy, particularly for regression of hepatic fibrosis or cirrhosis, reflecting the biological heterogeneity and dynamic cellular architecture of the disease. Distinct from conventional pathway- or drug class-based reviews, we summarize emerging therapeutics through a liver cell-centered framework, integrating hepatocyte-directed metabolic therapies, immune-cell modulation, hepatic stellate cell-targeted antifibrotic strategies, niche-directed approaches involving liver sinusoidal endothelial cells and cholangiocytes, systemic multi-cell modulators, and precision-delivery technologies. We further compare how these interventions reshape pathogenic communication among hepatic and extrahepatic compartments, while emphasizing unresolved challenges in drug target selection, cellular specificity, disease-stage dependency, safety, and patient stratification. This perspective emphasizes the need to move from isolated pathway targeting toward cell- and network-informed therapeutic strategies supported by spatial multi-omics, human-relevant models, and precision delivery.
PMID:42719321 | PMC:PMC13557022 | DOI:10.2147/DDDT.S543657
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cs.AI, q-bio.NC updates on arXiv.org
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Talking to Itself While Coding: What Makes Comments Help Code Generation?
arXiv:2609.09242v1 Announce Type: cross Abstract: Large Language Models (LLMs) often generate natural-language comments while writing code, and these comments become part of the context used to generate the code that follows. However, it remains unclear which properties of comments affect code-generation performance. We study this question through observational analyses and controlled interventions. On LiveCodeBench, neither comment frequency nor broad comment intent reliably predicts pass@1. W
Talking to Itself While Coding: What Makes Comments Help Code Generation?
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cs.AI, q-bio.NC updates on arXiv.org
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RAU: Reference-based Anatomical Understanding with Vision Language Models
arXiv:2509.22404v2 Announce Type: replace-cross Abstract: Anatomical understanding, which is the ability to identify, localize, or segment anatomical structures, is critical in medical image analysis; however, its progress is constrained by the scarcity of expert-labeled data. A promising remedy is to leverage an annotated reference image to guide the interpretation of an unlabeled target. Although recent vision-language models (VLMs) exhibit non-trivial visual reasoning, their reference-based
RAU: Reference-based Anatomical Understanding with Vision Language Models
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Oncogenesis - nature.com science feeds
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SHP1 expression in tumor-associated dendritic cells drives immunoevasion via impairing CD8<sup>+</sup> memory T cell responses
Oncogenesis, Published online: 15 May 2026; doi:10.1038/s41389-026-00627-zSHP1 expression in tumor-associated dendritic cells drives immunoevasion via impairing CD8+ memory T cell responses
SHP1 expression in tumor-associated dendritic cells drives immunoevasion via impairing CD8<sup>+</sup> memory T cell responses
Oncogenesis, Published online: 15 May 2026; doi:10.1038/s41389-026-00627-z
SHP1 expression in tumor-associated dendritic cells drives immunoevasion via impairing CD8+ memory T cell responses-
Omics in Gastric
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Machine learning-based identification of key genes underlying sex differences in hepatocellular carcinoma and targeted drug screening
Biomed Rep. 2026 Apr 24;24(6):74. doi: 10.3892/br.2026.2147. eCollection 2026 Jun.ABSTRACTHepatocellular carcinoma (HCC) shows a marked predominance in men, yet the molecular basis for this sex disparity remains unclear. The present study leveraged multi-omics data and machine learning algorithms to identify key genes associated with sex-specific differences in HCC and to screen for putative candidate compounds, aiming to provide new insights for sex-specific therapy. The mRNA expression data of
Machine learning-based identification of key genes underlying sex differences in hepatocellular carcinoma and targeted drug screening
Biomed Rep. 2026 Apr 24;24(6):74. doi: 10.3892/br.2026.2147. eCollection 2026 Jun.
ABSTRACT
Hepatocellular carcinoma (HCC) shows a marked predominance in men, yet the molecular basis for this sex disparity remains unclear. The present study leveraged multi-omics data and machine learning algorithms to identify key genes associated with sex-specific differences in HCC and to screen for putative candidate compounds, aiming to provide new insights for sex-specific therapy. The mRNA expression data of male and female patients with HCC and paracancerous tissues were obtained from the GEO and TCGA databases. To mitigate overfitting, data were partitioned into independent training and testing sets. Candidate genes were screened by differential expression analysis and weighted gene co-expression network analysis. A total of four complementary algorithms, random forest, support vector machines, generalized linear models and extreme gradient boosting were used to identify key genes with high predictive capability. CYP17A1 and IRX3 were identified as the top differentially expressed core genes associated with HCC in men. Pan-cancer analysis showed that CYP17A1 was lowly expressed in the majority of tumors, but significantly highly expressed in HCC, rectal adenocarcinoma and gastric cancer (P<0.001). Functional cell-based assays showed that knockout of CYP17A1 inhibited the proliferation, migration and invasion ability of HCC cells (P<0.001). Immunohistochemistry showed that CYP17A1 protein expression was significantly increased in HCC tissues from male patients when compared with that in paracancerous tissues (P<0.001), whereas there was no significant difference in female patient tissues (P>0.05). Notably, while IRX3 was identified computationally, its functional role remains to be experimentally validated. Molecular docking predicted a potential interaction between the natural compound Saikosaponin A and the CYP17A1 protein, and cellular assays revealed that it dose-dependently inhibits HCC cell malignant phenotypes. The present study suggests that CYP17A1 is associated with sex differences in HCC, potentially via the androgen signaling axis. Furthermore, IRX3 emerges as a novel hypothesis-generating candidate gene. Finally, the findings of the present study highlight Saikosaponin A as a putative therapeutic candidate for male patients with HCC, warranting further target-dependency investigations.
PMID:42125766 | PMC:PMC13158723 | DOI:10.3892/br.2026.2147
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cs.AI, q-bio.NC updates on arXiv.org
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Cardinality Estimation for High Dimensional Similarity Queries with Adaptive Bucket Probing
arXiv:2604.04603v1 Announce Type: cross Abstract: In this work, we address the problem of cardinality estimation for similarity search in high-dimensional spaces. Our goal is to design a framework that is lightweight, easy to construct, and capable of providing accurate estimates with satisfying online efficiency. We leverage locality-sensitive hashing (LSH) to partition the vector space while preserving distance proximity. Building on this, we adopt the principles of classical multi-probe LSH
Cardinality Estimation for High Dimensional Similarity Queries with Adaptive Bucket Probing
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cs.AI, q-bio.NC updates on arXiv.org
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Xpertbench: Expert Level Tasks with Rubrics-Based Evaluation
arXiv:2604.02368v3 Announce Type: replace Abstract: As Large Language Models (LLMs) exhibit plateauing performance on conventional benchmarks, a pivotal challenge persists: evaluating their proficiency in complex, open-ended tasks characterizing genuine expert-level cognition. Existing frameworks suffer from narrow domain coverage, reliance on generalist tasks, or self-evaluation biases. To bridge this gap, we present XpertBench, a high-fidelity benchmark engineered to assess LLMs across authen
Xpertbench: Expert Level Tasks with Rubrics-Based Evaluation
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cs.AI, q-bio.NC updates on arXiv.org
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Document Parsing Unveiled: Techniques, Challenges, and Prospects for Structured Information Extraction
arXiv:2410.21169v5 Announce Type: replace-cross Abstract: Document parsing (DP) transforms unstructured or semi-structured documents into structured, machine-readable representations, enabling downstream applications such as knowledge base construction and retrieval-augmented generation (RAG). This survey provides a comprehensive and timely review of document parsing research. We propose a systematic taxonomy that organizes existing approaches into modular pipeline-based systems and unified mod
Document Parsing Unveiled: Techniques, Challenges, and Prospects for Structured Information Extraction
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cs.AI, q-bio.NC updates on arXiv.org
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Security Considerations for Artificial Intelligence Agents
arXiv:2603.12230v2 Announce Type: replace-cross Abstract: This article, a lightly adapted version of Perplexity's response to NIST/CAISI Request for Information 2025-0035, details our observations and recommendations concerning the security of frontier AI agents. These insights are informed by Perplexity's experience operating general-purpose agentic systems used by millions of users and thousands of enterprises in both controlled and open-world environments. Agent architectures change core ass
Security Considerations for Artificial Intelligence Agents
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(Multiomics OR Omics) AND (Lung OR gastric OR Hepatocellular)
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Decoding macrophage heterogeneity in the pulmonary fibrosis lung cancer transition
Front Immunol. 2026 Mar 20;17:1787094. doi: 10.3389/fimmu.2026.1787094. eCollection 2026.ABSTRACTPulmonary fibrosis (PF) significantly increases the risk of lung cancer (LC), but the mechanisms underlying this transition remain unclear. This overview positions macrophage heterogeneity as a central node within the PF-LC continuum. First, we describe important subpopulations of profibrotic and pro-tumor macrophages, including SPP1+, MERTK+, TREM2+, and MARCO+ cells, using high-resolution spatial a
Decoding macrophage heterogeneity in the pulmonary fibrosis lung cancer transition
Front Immunol. 2026 Mar 20;17:1787094. doi: 10.3389/fimmu.2026.1787094. eCollection 2026.
ABSTRACT
Pulmonary fibrosis (PF) significantly increases the risk of lung cancer (LC), but the mechanisms underlying this transition remain unclear. This overview positions macrophage heterogeneity as a central node within the PF-LC continuum. First, we describe important subpopulations of profibrotic and pro-tumor macrophages, including SPP1+, MERTK+, TREM2+, and MARCO+ cells, using high-resolution spatial and single-cell omics technologies. Next, we analyze the fundamental mechanisms that determine their function: the fibrotic microenvironment (e.g., extracellular matrix stiffness, hypoxia) induces profound metabolic reprogramming (e.g., Warburg effect, lipid peroxidation) and stabilizes epigenetic memory (e.g., DNA methylation, histone modifications), locking them into a pathogenic state. This reprogramming occurs through two main pathways: (1) metabolic reprogramming, characterized by aerobic glycolytic conversion and dysregulated lipid metabolism, which stimulates both pathogenic functions and suppression of T cell activity; (2) Epigenetic modifications, including stabilized alterations in DNA methylation, histone modifications, and superactivator patterns, which maintain cells in a tumor-promoting phenotype. As central nodes of communication, these macrophages interact pathologically with fibroblasts and epithelial cells through secreted factors and extracellular vesicles, forming self-reinforcing feedback loops that promote disease progression. We are studying the crucial role of new technologies, particularly multi-omic spatial models and high-precision organoids, in fostering mechanistic discoveries. These discoveries pave the way for new macrophage-focused therapeutic strategies, including the precise stratification of patients using biomarkers from liquid biopsies (such as soluble SPP1 and MARCO) and the development of targeted drug delivery systems for the selective modulation of macrophage function, thus establishing a new paradigm for therapeutic interventions in pulmonary fibrosis with concomitant lung cancer.
PMID:41939908 | PMC:PMC13046558 | DOI:10.3389/fimmu.2026.1787094
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Omics In Lung
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Decoding macrophage heterogeneity in the pulmonary fibrosis lung cancer transition
Front Immunol. 2026 Mar 20;17:1787094. doi: 10.3389/fimmu.2026.1787094. eCollection 2026.ABSTRACTPulmonary fibrosis (PF) significantly increases the risk of lung cancer (LC), but the mechanisms underlying this transition remain unclear. This overview positions macrophage heterogeneity as a central node within the PF-LC continuum. First, we describe important subpopulations of profibrotic and pro-tumor macrophages, including SPP1+, MERTK+, TREM2+, and MARCO+ cells, using high-resolution spatial a
Decoding macrophage heterogeneity in the pulmonary fibrosis lung cancer transition
Front Immunol. 2026 Mar 20;17:1787094. doi: 10.3389/fimmu.2026.1787094. eCollection 2026.
ABSTRACT
Pulmonary fibrosis (PF) significantly increases the risk of lung cancer (LC), but the mechanisms underlying this transition remain unclear. This overview positions macrophage heterogeneity as a central node within the PF-LC continuum. First, we describe important subpopulations of profibrotic and pro-tumor macrophages, including SPP1+, MERTK+, TREM2+, and MARCO+ cells, using high-resolution spatial and single-cell omics technologies. Next, we analyze the fundamental mechanisms that determine their function: the fibrotic microenvironment (e.g., extracellular matrix stiffness, hypoxia) induces profound metabolic reprogramming (e.g., Warburg effect, lipid peroxidation) and stabilizes epigenetic memory (e.g., DNA methylation, histone modifications), locking them into a pathogenic state. This reprogramming occurs through two main pathways: (1) metabolic reprogramming, characterized by aerobic glycolytic conversion and dysregulated lipid metabolism, which stimulates both pathogenic functions and suppression of T cell activity; (2) Epigenetic modifications, including stabilized alterations in DNA methylation, histone modifications, and superactivator patterns, which maintain cells in a tumor-promoting phenotype. As central nodes of communication, these macrophages interact pathologically with fibroblasts and epithelial cells through secreted factors and extracellular vesicles, forming self-reinforcing feedback loops that promote disease progression. We are studying the crucial role of new technologies, particularly multi-omic spatial models and high-precision organoids, in fostering mechanistic discoveries. These discoveries pave the way for new macrophage-focused therapeutic strategies, including the precise stratification of patients using biomarkers from liquid biopsies (such as soluble SPP1 and MARCO) and the development of targeted drug delivery systems for the selective modulation of macrophage function, thus establishing a new paradigm for therapeutic interventions in pulmonary fibrosis with concomitant lung cancer.
PMID:41939908 | PMC:PMC13046558 | DOI:10.3389/fimmu.2026.1787094
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cs.AI, q-bio.NC updates on arXiv.org
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Countering Catastrophic Forgetting of Large Language Models for Better Instruction Following via Weight-Space Model Merging
arXiv:2604.01538v1 Announce Type: cross Abstract: Large language models have been adopted in the medical domain for clinical documentation to reduce clinician burden. However, studies have reported that LLMs often "forget" a significant amount of instruction-following ability when fine-tuned using a task-specific medical dataset, a critical challenge in adopting general-purpose LLMs for clinical applications. This study presents a model merging framework to efficiently adapt general-purpose LLM
Countering Catastrophic Forgetting of Large Language Models for Better Instruction Following via Weight-Space Model Merging
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Omics In Lung
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Catgut implantation at acupoints improves anti-PD-1 inhibitor efficacy in lung cancer by inducing immune responses and remodeling the tumor microenvironment
Cancer Immunol Immunother. 2026 Mar 31;75(4):126. doi: 10.1007/s00262-026-04368-1.ABSTRACTWhile anti-programmed death-1 (anti-PD-1) therapy has revolutionized lung cancer treatment, its efficacy remains limited by an immunosuppressive tumor microenvironment (TME). We therefore investigated whether combining anti-PD-1 inhibitor with catgut embedding at the Zusanli acupoint (CIAA) could enhance anti-tumor immunity by reprogramming the TME in a lung cancer mouse model. Combining in vivo tumor monit
Catgut implantation at acupoints improves anti-PD-1 inhibitor efficacy in lung cancer by inducing immune responses and remodeling the tumor microenvironment
Cancer Immunol Immunother. 2026 Mar 31;75(4):126. doi: 10.1007/s00262-026-04368-1.
ABSTRACT
While anti-programmed death-1 (anti-PD-1) therapy has revolutionized lung cancer treatment, its efficacy remains limited by an immunosuppressive tumor microenvironment (TME). We therefore investigated whether combining anti-PD-1 inhibitor with catgut embedding at the Zusanli acupoint (CIAA) could enhance anti-tumor immunity by reprogramming the TME in a lung cancer mouse model. Combining in vivo tumor monitoring, multi-parametric immune profiling (flow cytometry, IHC, ELISA), and multi-omics analyses (transcriptomics and metabolomics), we found that the combination therapy was associated with enhanced tumor growth inhibition. This effect correlated with a comprehensive TME transformation: conversion to an immunologically active state with increased effector immune cell infiltration (CD8⁺ T, CD4⁺ T, B cells, macrophages) and decreased regulatory T cells, coupled with suppression of pro-tumorigenic factors (VEGF, IL-6). Integrated omics analysis suggests that the combined treatment may modulate tumor-stroma interaction pathways (e.g., PI3K-Akt, focal adhesion) and rewire immunometabolic networks (e.g., tryptophan metabolism). Our study provides hypothesis-generating correlative data positioning CIAA as a potential adjunct capable of remodeling the TME to potentiate anti-PD-1 therapy in lung cancer.
PMID:41915222 | PMC:PMC13038699 | DOI:10.1007/s00262-026-04368-1
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(Multiomics OR Omics) AND (Lung OR gastric OR Hepatocellular)
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Catgut implantation at acupoints improves anti-PD-1 inhibitor efficacy in lung cancer by inducing immune responses and remodeling the tumor microenvironment
Cancer Immunol Immunother. 2026 Mar 31;75(4):126. doi: 10.1007/s00262-026-04368-1.ABSTRACTWhile anti-programmed death-1 (anti-PD-1) therapy has revolutionized lung cancer treatment, its efficacy remains limited by an immunosuppressive tumor microenvironment (TME). We therefore investigated whether combining anti-PD-1 inhibitor with catgut embedding at the Zusanli acupoint (CIAA) could enhance anti-tumor immunity by reprogramming the TME in a lung cancer mouse model. Combining in vivo tumor monit
Catgut implantation at acupoints improves anti-PD-1 inhibitor efficacy in lung cancer by inducing immune responses and remodeling the tumor microenvironment
Cancer Immunol Immunother. 2026 Mar 31;75(4):126. doi: 10.1007/s00262-026-04368-1.
ABSTRACT
While anti-programmed death-1 (anti-PD-1) therapy has revolutionized lung cancer treatment, its efficacy remains limited by an immunosuppressive tumor microenvironment (TME). We therefore investigated whether combining anti-PD-1 inhibitor with catgut embedding at the Zusanli acupoint (CIAA) could enhance anti-tumor immunity by reprogramming the TME in a lung cancer mouse model. Combining in vivo tumor monitoring, multi-parametric immune profiling (flow cytometry, IHC, ELISA), and multi-omics analyses (transcriptomics and metabolomics), we found that the combination therapy was associated with enhanced tumor growth inhibition. This effect correlated with a comprehensive TME transformation: conversion to an immunologically active state with increased effector immune cell infiltration (CD8⁺ T, CD4⁺ T, B cells, macrophages) and decreased regulatory T cells, coupled with suppression of pro-tumorigenic factors (VEGF, IL-6). Integrated omics analysis suggests that the combined treatment may modulate tumor-stroma interaction pathways (e.g., PI3K-Akt, focal adhesion) and rewire immunometabolic networks (e.g., tryptophan metabolism). Our study provides hypothesis-generating correlative data positioning CIAA as a potential adjunct capable of remodeling the TME to potentiate anti-PD-1 therapy in lung cancer.
PMID:41915222 | DOI:10.1007/s00262-026-04368-1
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Omics In Lung
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A monocyte-centered framework for predicting immunochemotherapy efficacy in lung squamous cell carcinoma patients
EMBO Mol Med. 2026 Mar 30. doi: 10.1038/s44321-026-00410-y. Online ahead of print.ABSTRACTLung cancer is the leading cause of cancer-related mortality worldwide, with lung squamous cell carcinoma (LUSC) comprising 20-30% of cases. Immunochemotherapy (IC) is the standard first-line treatment for advanced LUSC, yet reliable predictors of therapeutic response remain unavailable. Using single-cell multi-omics profiling of paired pre- and post-treatment tumor and blood samples, we observed that patie
A monocyte-centered framework for predicting immunochemotherapy efficacy in lung squamous cell carcinoma patients
EMBO Mol Med. 2026 Mar 30. doi: 10.1038/s44321-026-00410-y. Online ahead of print.
ABSTRACT
Lung cancer is the leading cause of cancer-related mortality worldwide, with lung squamous cell carcinoma (LUSC) comprising 20-30% of cases. Immunochemotherapy (IC) is the standard first-line treatment for advanced LUSC, yet reliable predictors of therapeutic response remain unavailable. Using single-cell multi-omics profiling of paired pre- and post-treatment tumor and blood samples, we observed that patients responding to IC exhibited significantly higher baseline levels of peripheral blood monocytes, tumor-infiltrating classical monocytes, and APOBEC3A+ monocytes across both compartments compared with non-responders. These associations were independently validated in additional cohorts using routine complete blood count testing and multiplex immunofluorescence analysis of native tumor tissues. Our findings reveal monocyte-related parameters as clinically accessible indicators that link systemic immunity with the tumor microenvironment and hold promise for predicting IC responsiveness in patients with LUSC.
PMID:41912871 | DOI:10.1038/s44321-026-00410-y
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(Multiomics OR Omics) AND (Lung OR gastric OR Hepatocellular)
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A monocyte-centered framework for predicting immunochemotherapy efficacy in lung squamous cell carcinoma patients
EMBO Mol Med. 2026 Mar 30. doi: 10.1038/s44321-026-00410-y. Online ahead of print.ABSTRACTLung cancer is the leading cause of cancer-related mortality worldwide, with lung squamous cell carcinoma (LUSC) comprising 20-30% of cases. Immunochemotherapy (IC) is the standard first-line treatment for advanced LUSC, yet reliable predictors of therapeutic response remain unavailable. Using single-cell multi-omics profiling of paired pre- and post-treatment tumor and blood samples, we observed that patie
A monocyte-centered framework for predicting immunochemotherapy efficacy in lung squamous cell carcinoma patients
EMBO Mol Med. 2026 Mar 30. doi: 10.1038/s44321-026-00410-y. Online ahead of print.
ABSTRACT
Lung cancer is the leading cause of cancer-related mortality worldwide, with lung squamous cell carcinoma (LUSC) comprising 20-30% of cases. Immunochemotherapy (IC) is the standard first-line treatment for advanced LUSC, yet reliable predictors of therapeutic response remain unavailable. Using single-cell multi-omics profiling of paired pre- and post-treatment tumor and blood samples, we observed that patients responding to IC exhibited significantly higher baseline levels of peripheral blood monocytes, tumor-infiltrating classical monocytes, and APOBEC3A+ monocytes across both compartments compared with non-responders. These associations were independently validated in additional cohorts using routine complete blood count testing and multiplex immunofluorescence analysis of native tumor tissues. Our findings reveal monocyte-related parameters as clinically accessible indicators that link systemic immunity with the tumor microenvironment and hold promise for predicting IC responsiveness in patients with LUSC.
PMID:41912871 | DOI:10.1038/s44321-026-00410-y
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cs.AI, q-bio.NC updates on arXiv.org
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Residual Decoding: Mitigating Hallucinations in Large Vision-Language Models via History-Aware Residual Guidance
arXiv:2602.01047v3 Announce Type: replace-cross Abstract: Large Vision-Language Models (LVLMs) can reason from image-text inputs and perform well in various multimodal tasks. Despite this success, they are affected by language priors and often produce hallucinations. Hallucinations denote generated content that is grammatically and syntactically coherent, yet bears no match or direct relevance to visual input. To address this problem, we propose Residual Decoding (ResDec). It is a novel trainin