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cs.AI, q-bio.NC updates on arXiv.org
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Agent-as-Peer-Debriefer: A Multi-Agent Framework with Perspective-Based Refinement for Qualitative Analysis
arXiv:2605.24600v1 Announce Type: new Abstract: Large language models (LLMs) are increasingly used for qualitative data analysis (QDA), yet their outputs often miss the depth and nuance of human analysis. We argue this gap reflects a missing credibility practice from human QDA: peer debriefing, in which an analyst seeks feedback from a disinterested peer and uses it to refine their coding. To bring this practice into LLM-assisted QDA, we propose Agent-as-Peer-Debriefer, a multi-agent QDA framew
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Oncogene - Issue - nature.com science feeds
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GPX8<sup>+</sup> cancer-associated fibroblast-derived lactate contributes to lenvatinib resistance by facilitating BRPF1 expression through histone H3 lysine 18 lactylation in hepatocellular carcinoma
Oncogene, Published online: 22 May 2026; doi:10.1038/s41388-026-03711-1GPX8+ cancer-associated fibroblast-derived lactate contributes to lenvatinib resistance by facilitating BRPF1 expression through histone H3 lysine 18 lactylation in hepatocellular carcinoma
GPX8<sup>+</sup> cancer-associated fibroblast-derived lactate contributes to lenvatinib resistance by facilitating BRPF1 expression through histone H3 lysine 18 lactylation in hepatocellular carcinoma
Oncogene, Published online: 22 May 2026; doi:10.1038/s41388-026-03711-1
GPX8+ cancer-associated fibroblast-derived lactate contributes to lenvatinib resistance by facilitating BRPF1 expression through histone H3 lysine 18 lactylation in hepatocellular carcinoma-
AAAS: Table of Contents
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Induction of broadly neutralizing HIV antibodies by a two-step mechanism informs vaccine design
Science, Ahead of Print.
Induction of broadly neutralizing HIV antibodies by a two-step mechanism informs vaccine design
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Oncogene - Issue - nature.com science feeds
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Granzyme B-based CAR-T cells targeting membrane-bound HSP70 suppress solid tumor growth and metastasis
Oncogene, Published online: 18 April 2026; doi:10.1038/s41388-026-03797-7Granzyme B-based CAR-T cells targeting membrane-bound HSP70 suppress solid tumor growth and metastasis
Granzyme B-based CAR-T cells targeting membrane-bound HSP70 suppress solid tumor growth and metastasis
Oncogene, Published online: 18 April 2026; doi:10.1038/s41388-026-03797-7
Granzyme B-based CAR-T cells targeting membrane-bound HSP70 suppress solid tumor growth and metastasis-
Omics In Lung
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Applications and challenges of multi-omics approaches in lung cancer research and precision treatment
Front Genet. 2026 Mar 23;16:1722368. doi: 10.3389/fgene.2025.1722368. eCollection 2025.ABSTRACTLung cancer is one of the most common cancers worldwide and one of the leading causes of cancer death, with a heavy disease burden and severe public health challenges. Multi-omics techniques, such as genomics, proteomics, metabolomics, and radiomics, play a crucial role in the early diagnosis and treatment of lung cancer, revealing the molecular characteristics and mechanisms of lung cancer, and have s
Applications and challenges of multi-omics approaches in lung cancer research and precision treatment
Front Genet. 2026 Mar 23;16:1722368. doi: 10.3389/fgene.2025.1722368. eCollection 2025.
ABSTRACT
Lung cancer is one of the most common cancers worldwide and one of the leading causes of cancer death, with a heavy disease burden and severe public health challenges. Multi-omics techniques, such as genomics, proteomics, metabolomics, and radiomics, play a crucial role in the early diagnosis and treatment of lung cancer, revealing the molecular characteristics and mechanisms of lung cancer, and have significant clinical application value. However, it also faces numerous challenges, such as data issues, "black box" problems, and ethical and legal concerns. How to leverage strengths while mitigating weaknesses, achieve clinical translation of technology, and serve patients more effectively deserves our deep reflection. This article reviews the specific applications and challenges of multi-omics methods in lung cancer research and personalized treatment.
PMID:41948518 | PMC:PMC13050793 | DOI:10.3389/fgene.2025.1722368
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Nature - Issue - nature.com science feeds
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Engineered immunosuppressive dendritic cells protect against cardiac remodelling
Nature, Published online: 08 April 2026; doi:10.1038/s41586-026-10346-5Lesion-targeted immune modulation is a feasible strategy to control cardiac fibrosis, and engineered dendritic cells are a promising therapeutic platform for treating cardiac remodelling and heart failure.
Engineered immunosuppressive dendritic cells protect against cardiac remodelling
Nature, Published online: 08 April 2026; doi:10.1038/s41586-026-10346-5
Lesion-targeted immune modulation is a feasible strategy to control cardiac fibrosis, and engineered dendritic cells are a promising therapeutic platform for treating cardiac remodelling and heart failure.-
Oncogene - Issue - nature.com science feeds
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<i>Fusobacterium nucleatum</i> drives colorectal cancer progression through the <i>circPTBP</i>3/<i>miR-760</i>/<i>PUM1</i> axis
Oncogene, Published online: 31 March 2026; doi:10.1038/s41388-026-03746-4Fusobacterium nucleatum drives colorectal cancer progression through the circPTBP3/miR-760/PUM1 axis
<i>Fusobacterium nucleatum</i> drives colorectal cancer progression through the <i>circPTBP</i>3/<i>miR-760</i>/<i>PUM1</i> axis
Oncogene, Published online: 31 March 2026; doi:10.1038/s41388-026-03746-4
Fusobacterium nucleatum drives colorectal cancer progression through the circPTBP3/miR-760/PUM1 axis-
(Multiomics OR Omics) AND (Lung OR gastric OR Hepatocellular)
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RFC4 drives temozolomide resistance in glioblastoma by activating STK38-BECN1-dependent autophagy
Nat Commun. 2026 Mar 23. doi: 10.1038/s41467-026-70798-1. Online ahead of print.ABSTRACTGlioblastoma (GBM) remains a lethal brain tumor due to therapy resistance. While autophagy contributes to temozolomide (TMZ) resistance, its regulation is incompletely understood. This study investigates the role of replication factor RFC4, which is associated with poor prognosis and TMZ resistance in GBM. Multi-omics analyses and molecular experiments reveal that TMZ-induced chromatin accessibility enables t
RFC4 drives temozolomide resistance in glioblastoma by activating STK38-BECN1-dependent autophagy
Nat Commun. 2026 Mar 23. doi: 10.1038/s41467-026-70798-1. Online ahead of print.
ABSTRACT
Glioblastoma (GBM) remains a lethal brain tumor due to therapy resistance. While autophagy contributes to temozolomide (TMZ) resistance, its regulation is incompletely understood. This study investigates the role of replication factor RFC4, which is associated with poor prognosis and TMZ resistance in GBM. Multi-omics analyses and molecular experiments reveal that TMZ-induced chromatin accessibility enables transcription factor YY1 to bind the RFC4 promoter and upregulate its expression. RFC4, in turn, stabilizes the kinase STK38, which is essential for autophagosome formation. The RFC4-STK38 interaction facilitates BECN1 recruitment, thereby activating autophagy. Phosphorylation of STK38 at T444 stabilizes this complex, whereas a phospho-deficient mutant impairs autophagy. In vivo, RFC4 overexpression confers TMZ resistance, reversible by autophagy inhibition. Thus, our findings identify the RFC4-STK38-BECN1 axis as a mechanism underlying TMZ resistance and a potential target for precision therapy in GBM.
PMID:41872171 | DOI:10.1038/s41467-026-70798-1
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(Multiomics OR Omics) AND (Lung OR gastric OR Hepatocellular)
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Unannotated noncoding transcripts as a source of intratumor heterogeneity in malignant cell states
Sci China Life Sci. 2026 Mar 16. doi: 10.1007/s11427-025-3273-6. Online ahead of print.ABSTRACTPhenotypic diversity of malignant cells within a tumor underlies intratumor heterogeneity (ITH), a key determinant of cancer metastasis and treatment failure. However, the molecular mechanisms driving this heterogeneity are poorly understood. Here, we curated and analyzed a cohort of 3' tag-based single-cell RNA-seq covering 12 common cancer types. We identified thousands of poly(A) site (PAS) peaks re
Unannotated noncoding transcripts as a source of intratumor heterogeneity in malignant cell states
Sci China Life Sci. 2026 Mar 16. doi: 10.1007/s11427-025-3273-6. Online ahead of print.
ABSTRACT
Phenotypic diversity of malignant cells within a tumor underlies intratumor heterogeneity (ITH), a key determinant of cancer metastasis and treatment failure. However, the molecular mechanisms driving this heterogeneity are poorly understood. Here, we curated and analyzed a cohort of 3' tag-based single-cell RNA-seq covering 12 common cancer types. We identified thousands of poly(A) site (PAS) peaks representing the 3' ends of previously unannotated transcripts, whose expression is widely associated with diverse malignant cellular states. By integrating multi-omics data, we characterized the expression patterns and epigenetic landscape of these unannotated PAS peak-associated transcripts (UPTs). The expression heterogeneity of UPTs was supported by multi-region sampling bulk RNA-seq data and recapitulated within cancer cell lines. As proof of principle validation, functional experiments confirmed that two noncoding UPTs promoted the proliferation and migration of lung cancer cells. Our results suggest that epigenetic activation of unannotated noncoding transcripts might represent a previously unrecognized mechanism contributing to transcriptomic ITH.
PMID:41870780 | DOI:10.1007/s11427-025-3273-6
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Omics In Lung
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Unannotated noncoding transcripts as a source of intratumor heterogeneity in malignant cell states
Sci China Life Sci. 2026 Mar 16. doi: 10.1007/s11427-025-3273-6. Online ahead of print.ABSTRACTPhenotypic diversity of malignant cells within a tumor underlies intratumor heterogeneity (ITH), a key determinant of cancer metastasis and treatment failure. However, the molecular mechanisms driving this heterogeneity are poorly understood. Here, we curated and analyzed a cohort of 3' tag-based single-cell RNA-seq covering 12 common cancer types. We identified thousands of poly(A) site (PAS) peaks re
Unannotated noncoding transcripts as a source of intratumor heterogeneity in malignant cell states
Sci China Life Sci. 2026 Mar 16. doi: 10.1007/s11427-025-3273-6. Online ahead of print.
ABSTRACT
Phenotypic diversity of malignant cells within a tumor underlies intratumor heterogeneity (ITH), a key determinant of cancer metastasis and treatment failure. However, the molecular mechanisms driving this heterogeneity are poorly understood. Here, we curated and analyzed a cohort of 3' tag-based single-cell RNA-seq covering 12 common cancer types. We identified thousands of poly(A) site (PAS) peaks representing the 3' ends of previously unannotated transcripts, whose expression is widely associated with diverse malignant cellular states. By integrating multi-omics data, we characterized the expression patterns and epigenetic landscape of these unannotated PAS peak-associated transcripts (UPTs). The expression heterogeneity of UPTs was supported by multi-region sampling bulk RNA-seq data and recapitulated within cancer cell lines. As proof of principle validation, functional experiments confirmed that two noncoding UPTs promoted the proliferation and migration of lung cancer cells. Our results suggest that epigenetic activation of unannotated noncoding transcripts might represent a previously unrecognized mechanism contributing to transcriptomic ITH.
PMID:41870780 | DOI:10.1007/s11427-025-3273-6
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Omics In Lung
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Low-dose intestinal irradiation enhances the efficacy and prognosis of PD-1 blockade in metastatic non-small cell lung cancer
Clin Cancer Res. 2026 Mar 18. doi: 10.1158/1078-0432.CCR-25-4153. Online ahead of print.ABSTRACTPURPOSE: Intestinal low-dose irradiation (ILDR) may enhance immunotherapy efficacy by modulating the gut microbiota and metabolism; however, its role in metastatic non-small cell lung cancer (mNSCLC), particularly in the first-line setting, remains unclear.EXPERIMENTAL DESIGN: This multicenter retrospective and prospective study included mNSCLC patients receiving first- and second-line programmed cell
Low-dose intestinal irradiation enhances the efficacy and prognosis of PD-1 blockade in metastatic non-small cell lung cancer
Clin Cancer Res. 2026 Mar 18. doi: 10.1158/1078-0432.CCR-25-4153. Online ahead of print.
ABSTRACT
PURPOSE: Intestinal low-dose irradiation (ILDR) may enhance immunotherapy efficacy by modulating the gut microbiota and metabolism; however, its role in metastatic non-small cell lung cancer (mNSCLC), particularly in the first-line setting, remains unclear.
EXPERIMENTAL DESIGN: This multicenter retrospective and prospective study included mNSCLC patients receiving first- and second-line programmed cell death protein 1 (PD-1) inhibitors along with abdominopelvic radiotherapy between 2018 and 2025. Patients were stratified by the mean intestinal radiation dose into <1 Gy, 1-3 Gy, and >3 Gy groups and treatment outcomes were compared. The blood and fecal samples were subjected to multi-omics profiling.
RESULTS: g>309 patients were included in the retrospective analysis. Optimal efficacy was observed with a small intestinal mean radiation dose (SIMRD) of 1-3 Gy, showing longer progression-free survival (PFS, 10.2 months) and overall survival (OS, 22.8 months) (P < 0.01), which was consistent across subgroups. Compared with 1-3 Gy, SIMRD >3 Gy (Hazard ratio [HR] = 4.87, P < 0.001) and <1 Gy (HR = 1.85, P < 0.001) independently predicted worse OS. Prospective results confirmed the best disease control rate (P = 0.041) and PFS (P = 0.046) with SIMRD of 1-3 Gy. Responders were enriched in Bacillota, Clostridia, and indole derivatives, particularly indole-3-carboxylic acid. Moreover, the 1-3 Gy group exhibited increased circulating macrophage inflammatory protein-3α and reduced circulating α4β7+ regulatory T cells.
CONCLUSIONS: ILDR influences the efficacy of PD-1 blockade in patients with mNSCLC, particularly when SIMRD is maintained within the 1-3 Gy range, likely through modulation of the gut microbiota-metabolite-immune axis.
PMID:41849236 | DOI:10.1158/1078-0432.CCR-25-4153
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cs.AI, q-bio.NC updates on arXiv.org
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Continual Learning in Large Language Models: Methods, Challenges, and Opportunities
arXiv:2603.12658v1 Announce Type: cross Abstract: Continual learning (CL) has emerged as a pivotal paradigm to enable large language models (LLMs) to dynamically adapt to evolving knowledge and sequential tasks while mitigating catastrophic forgetting-a critical limitation of the static pre-training paradigm inherent to modern LLMs. This survey presents a comprehensive overview of CL methodologies tailored for LLMs, structured around three core training stages: continual pre-training, continual
Continual Learning in Large Language Models: Methods, Challenges, and Opportunities
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cs.AI, q-bio.NC updates on arXiv.org
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OffTopicEval: When Large Language Models Enter the Wrong Chat, Almost Always!
arXiv:2509.26495v3 Announce Type: replace Abstract: Large Language Model (LLM) safety is one of the most pressing challenges for enabling wide-scale deployment. While most studies and global discussions focus on generic harms, such as models assisting users in harming themselves or others, enterprises face a more fundamental concern: whether LLM-based agents are safe for their intended use case. To address this, we introduce operational safety, defined as an LLM's ability to appropriately accep
OffTopicEval: When Large Language Models Enter the Wrong Chat, Almost Always!
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cs.AI, q-bio.NC updates on arXiv.org
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SkillsBench: Benchmarking How Well Agent Skills Work Across Diverse Tasks
arXiv:2602.12670v3 Announce Type: replace Abstract: Agent Skills are structured packages of procedural knowledge that augment LLM agents at inference time. Despite rapid adoption, there is no standard way to measure whether they actually help. We present SkillsBench, a benchmark of 86 tasks across 11 domains paired with curated Skills and deterministic verifiers. Each task is evaluated under three conditions: no Skills, curated Skills, and self-generated Skills. We test 7 agent-model configurat
SkillsBench: Benchmarking How Well Agent Skills Work Across Diverse Tasks
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Nature - Issue - nature.com science feeds
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Author Correction: Gut stem cell necroptosis by genome instability triggers bowel inflammation
Nature, Published online: 11 March 2026; doi:10.1038/s41586-026-10302-3Author Correction: Gut stem cell necroptosis by genome instability triggers bowel inflammation
Author Correction: Gut stem cell necroptosis by genome instability triggers bowel inflammation
Nature, Published online: 11 March 2026; doi:10.1038/s41586-026-10302-3
Author Correction: Gut stem cell necroptosis by genome instability triggers bowel inflammation-
cs.AI, q-bio.NC updates on arXiv.org
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SkillsBench: Benchmarking How Well Agent Skills Work Across Diverse Tasks
arXiv:2602.12670v2 Announce Type: replace Abstract: Agent Skills are structured packages of procedural knowledge that augment LLM agents at inference time. Despite rapid adoption, there is no standard way to measure whether they actually help. We present SkillsBench, a benchmark of 86 tasks across 11 domains paired with curated Skills and deterministic verifiers. Each task is evaluated under three conditions: no Skills, curated Skills, and self-generated Skills. We test 7 agent-model configurat
SkillsBench: Benchmarking How Well Agent Skills Work Across Diverse Tasks
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Cell Death Discovery nature.com science feeds
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Oscillatory shear stress-driven endothelial-to-mesenchymal transition: a critical mechanical signal transduction mechanism in atherosclerosis progression
Cell Death Discovery, Published online: 10 March 2026; doi:10.1038/s41420-026-03000-6Oscillatory shear stress-driven endothelial-to-mesenchymal transition: a critical mechanical signal transduction mechanism in atherosclerosis progression
Oscillatory shear stress-driven endothelial-to-mesenchymal transition: a critical mechanical signal transduction mechanism in atherosclerosis progression
Cell Death Discovery, Published online: 10 March 2026; doi:10.1038/s41420-026-03000-6
Oscillatory shear stress-driven endothelial-to-mesenchymal transition: a critical mechanical signal transduction mechanism in atherosclerosis progression-
cs.AI, q-bio.NC updates on arXiv.org
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Intelligent Pathological Diagnosis of Gestational Trophoblastic Diseases via Visual-Language Deep Learning Model
arXiv:2603.02704v1 Announce Type: cross Abstract: The pathological diagnosis of gestational trophoblastic disease(GTD) takes a long time, relies heavily on the experience of pathologists, and the consistency of initial diagnosis is low, which seriously threatens maternal health and reproductive outcomes. We developed an expert model for GTD pathological diagnosis, named GTDoctor. GTDoctor can perform pixel-based lesion segmentation on pathological slides, and output diagnostic conclusions and p