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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 the SFT loss according to the logit gap between the gold token and its strongest competitor. TrimSFT trims supervision away from both extremes: tokens already mastered (large logit gap) and tokens weakly supported by the current model (small or negative logit gap), concentrating learning within an intermediate logit-gap region between them. We instantiate this principle with a Gaussian weight centered at margin m with bandwidth {\tau}, requiring no reference model or additional forward pass. We evaluate TrimSFT on six base models from the Llama, Qwen, and DeepMath families across five mathematical reasoning benchmarks. TrimSFT consistently improves over standard SFT, achieving the best average performance on five out of six models, with gains of up to +26.9 points over SFT on MATH500. Further analyses show that the bandwidth {\tau} matters more than the exact margin location, and that half-trim variants that remove supervision pressure from only one side yield inferior trade-offs. A token-level logit-gap distribution analysis suggests that TrimSFT reshapes model confidence in a more balanced way than uniform SFT or monotonic reweighting methods. These results suggest that reasoning SFT can benefit from trimming both extremes rather than treating all tokens uniformly.
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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 training-free and model-agnostic framework for defending against structural attacks. KCES is built upon Graph Kernel Complexity (GKC), a principled metric derived from the graph Gram matrix that appears in a generalization upper bound on the GNN test error. From this bound, we define an edge-specific KC score that quantifies each edge's structural influence via its induced change in GKC. KCES then identifies and prunes high-KC edges, which are empirically enriched with adversarial perturbations under structural attacks, to mitigate their harmful impact. Computationally efficient and scalable, KCES operates as a lightweight preprocessing step without retraining and can be seamlessly integrated with existing defenses. Extensive experiments demonstrate that KCES consistently outperforms representative robust baselines across diverse attack settings and scales effectively to large graphs. Supported by theoretical analysis and extensive empirical validation, KCES provides a principled and efficient framework for securing GNNs. Our code is available at https://github.com/karpning/KCScore.
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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.

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-Ξ² 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-Ξ² activity, impaired Treg function, and enhanced antitumor immune responses in vivo. Collectively, these findings identify oncogenic KRAS as a key regulator of TGF-Ξ²-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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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
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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.

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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