Normal view
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cs.AI, q-bio.NC updates on arXiv.org
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Which Tokens Should SFT Actually Learn? A Token-Trimming Perspective on Mathematical Reasoning
arXiv:2609.09707v1 Announce Type: new Abstract: Supervised fine-tuning (SFT) applies a uniform cross-entropy loss to all target tokens, even though different tokens provide unequal learning signals for mathematical reasoning. This uniform treatment can over-sharpen already mastered tokens while amplifying learning pressure on uncertain, low-confidence tokens, leading to suboptimal training dynamics. We propose Trimmed Logit-Gap SFT (TrimSFT), a simple token-level reweighting method that scales
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cs.AI, q-bio.NC updates on arXiv.org
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Kernel-Complexity Edge Sanitization for Training-Free Defense against Structural Graph Attacks
arXiv:2609.09698v1 Announce Type: cross Abstract: Graph Neural Networks (GNNs) have achieved remarkable success across diverse applications, yet they remain highly vulnerable to adversarial attacks that maliciously perturb graph structure. Existing defenses often lack rigorous theoretical grounding, rely on attack-specific heuristics, or require costly retraining procedures such as adversarial training. To address these limitations, we propose Kernel-Complexity Edge Sanitization (KCES), a train
Kernel-Complexity Edge Sanitization for Training-Free Defense against Structural Graph Attacks
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(Multiomics OR Omics) AND (Lung OR gastric OR Hepatocellular)
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Targeting KRAS reprograms a Treg-dominant immunosuppressive microenvironment and sensitizes KRAS-mutant gastric adenocarcinoma to CTLA-4 immunotherapy
Sci China Life Sci. 2026 Sep 3. doi: 10.1007/s11427-026-3438-4. Online ahead of print.ABSTRACTOncogenic KRAS mutations define a distinct molecular subset of gastric adenocarcinoma (GA), yet their impact on the tumor immune microenvironment remains incompletely understood. In this study, we established a genetically faithful and immunocompetent KRASG12D-driven mouse model of GA, together with matched organoids and cell lines, to investigate how oncogenic KRAS shapes tumor-immune interactions. KRA
Targeting KRAS reprograms a Treg-dominant immunosuppressive microenvironment and sensitizes KRAS-mutant gastric adenocarcinoma to CTLA-4 immunotherapy
Sci China Life Sci. 2026 Sep 3. doi: 10.1007/s11427-026-3438-4. Online ahead of print.
ABSTRACT
Oncogenic KRAS mutations define a distinct molecular subset of gastric adenocarcinoma (GA), yet their impact on the tumor immune microenvironment remains incompletely understood. In this study, we established a genetically faithful and immunocompetent KRASG12D-driven mouse model of GA, together with matched organoids and cell lines, to investigate how oncogenic KRAS shapes tumor-immune interactions. KRAS-mutant tumors consistently developed an immunosuppressive microenvironment characterized by enrichment of regulatory T cells (Tregs), accompanied by reduced cytotoxic lymphocyte infiltration and intrinsic resistance to PD-1 blockade. Although pharmacologic targeting of KRAS effectively suppressed tumor growth and increased immune cell infiltration, functional immune analyses revealed persistent Treg-mediated immunosuppression that limited effective antitumor immunity. Mechanistically, TGF-β signaling was required to maintain Treg dominance and suppress effector T cell function in KRAS-driven tumors. Importantly, disruption of this suppressive axis through combined KRAS inhibition and CTLA-4 blockade attenuated TGF-β activity, impaired Treg function, and enhanced antitumor immune responses in vivo. Collectively, these findings identify oncogenic KRAS as a key regulator of TGF-β-dependent immune suppression in GA and provide mechanistic insight into immune evasion within this molecular subtype.
PMID:42714795 | DOI:10.1007/s11427-026-3438-4
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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 Gastric
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Cellular Senescence in Gastric Cancer: Molecular Mechanisms, Microenvironment Remodeling and Therapeutic Implications
Aging Dis. 2026 Mar 19. doi: 10.14336/AD.2025.1571. Online ahead of print.ABSTRACTGastric cancer (GC) remains a leading cause of cancer-related morbidity and mortality worldwide, with poor prognosis for advanced-stage patients. Therefore, in-depth exploration of the mechanisms underlying GC initiation and progression, as well as the development of novel therapeutic strategies, is of crucial importance. Cellular senescence is a stable cell cycle arrest program that plays a dual role in GC. It exe
Cellular Senescence in Gastric Cancer: Molecular Mechanisms, Microenvironment Remodeling and Therapeutic Implications
Aging Dis. 2026 Mar 19. doi: 10.14336/AD.2025.1571. Online ahead of print.
ABSTRACT
Gastric cancer (GC) remains a leading cause of cancer-related morbidity and mortality worldwide, with poor prognosis for advanced-stage patients. Therefore, in-depth exploration of the mechanisms underlying GC initiation and progression, as well as the development of novel therapeutic strategies, is of crucial importance. Cellular senescence is a stable cell cycle arrest program that plays a dual role in GC. It exerts tumor-suppressive effects via growth arrest but also promotes tumor progression and immune evasion by remodeling the tumor microenvironment (TME) through senescence-associated secretory phenotype (SASP). This review comprehensively elucidates the molecular mechanisms of cellular senescence in GC and the core regulatory networks involving gene regulation, epigenetic modifications, metabolic reprogramming, and cell cycle arrest. Additionally, the review highlights how senescent cells foster an immunosuppressive microenvironment via SASP, forming a self-reinforcing feed-forward loop. Regarding therapeutic strategies, we summarize potential approaches targeting cellular senescence, including senescence induction, senescent cell clearance, SASP modulation, and multi-target synergistic therapy by integrating epigenetic regulation, metabolic intervention, and immune microenvironment modulation. Despite progress, numerous challenges remain. Future studies should leverage multi-omics technologies, novel models' development, and large-scale clinical trials to advance the clinical translation of GC cellular senescence research, providing new insights for improving prognosis.
PMID:41910653 | DOI:10.14336/AD.2025.1571
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Nature - Issue - nature.com science feeds
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Direct conversion from alkenes to alkynes
Nature, Published online: 16 March 2026; doi:10.1038/s41586-026-10372-3Direct conversion from alkenes to alkynes
Direct conversion from alkenes to alkynes
Nature, Published online: 16 March 2026; doi:10.1038/s41586-026-10372-3
Direct conversion from alkenes to alkynes