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cs.AI, q-bio.NC updates on arXiv.org
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From Rubrics to Reliable Scores: Evidence-Grounded Text Evaluation with LLM Judges
arXiv:2601.08654v3 Announce Type: replace-cross Abstract: Rubric-based text evaluation increasingly relies on large language models (LLMs) as scalable judges, yet frozen black-box models can interpret the same criteria inconsistently, produce score attributions that are difficult to audit, and map judgments poorly onto human scoring scales. We define this challenge as criteria transfer: translating human rubric intent into a stable, auditable inference-time scoring protocol. We introduce Rulers
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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-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