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Reasoning as an Attack Surface: Adaptive Evolutionary CoT Jailbreaks for LLMs
ProActor: Timing-Aware Reinforcement Learning for Proactive Task Scheduling Agents
CODESKILL: Learning Self-Evolving Skills for Coding Agents
STREAM: A Data-Centric Framework for Mining High-Value Task-Oriented Dialogues from Streaming Media
NPSolver: Neural Poisson Solver with Iterative Physics Supervision
OASIS: Observation-Action Space Alignment via SE(3) Trajectory Prediction for Robotic Manipulation
Voting with the Graph: Stable RLAIF via Topological Consistency Maximization
PathMem: Toward Cognition-Aligned Memory Transformation for Pathology MLLMs
Topology-Driven Transferability Estimation of Medical Foundation Models for Segmentation
Cooperative Memory Paging with Keyword Bookmarks for Long-Horizon LLM Conversations
Depth Registers Unlock W4A4 on SwiGLU: A Reader/Generator Decomposition
Copy-as-Decode: Grammar-Constrained Parallel Prefill for LLM Editing
Committed SAE-Feature Traces for Audited-Session Substitution Detection in Hosted LLMs
Chain of Evidence: Pixel-Level Visual Attribution for Iterative Retrieval-Augmented Generation
Exploring the prognostic role of senescence-related genes in gastric cancer through multi-omics integration and machine learning
Hum Genomics. 2026 May 9. doi: 10.1186/s40246-026-00979-y. Online ahead of print.
ABSTRACT
Cellular senescence plays a context-dependent role in gastric cancer (GC), functioning both through tumor-suppressive arrest and the tumor-promoting senescence-associated secretory phenotype. However, its systematic integration into prognostic models remains limited. Here, we develop a novel interpretable framework to identify and validate a robust senescence-related gene signature for GC prognosis. We first introduce a dual-model interpretable feature selection strategy that integrates a biologically informed Kolmogorov-Arnold Network with a tabular foundation model to identify cancer-associated senescence genes. From the initial candidates, an ensemble of ten machine learning algorithms distills a core 4-gene signature to construct a Senescence Risk Score (SRS). The SRS proves to be a powerful and independent prognostic indicator, effectively stratifies patients into high- and low-risk groups with distinct overall survival across multiple cohorts. High-risk patients exhibit an "immune-hot" but potentially dysfunctional tumor microenvironment, characterized by enriched immune cell infiltration, elevated checkpoint expression, and distinct metabolic reprogramming favoring pathways such as angiogenesis and epithelial-mesenchymal transition (EMT). Furthermore, the SRS correlates with differential somatic mutation profiles and suggests potential sensitivity to specific chemotherapeutic agents. In vitro functional assays confirmed the oncogenic role of SERPINE1, a top-ranked core gene, in promoting GC cell proliferation. Regulatory network analysis revealed potential upstream transcription factors and miRNAs governing the signature. Collectively, we present a validated senescence-related prognostic signature that enables effective risk stratification of patients with gastric cancer.
PMID:42106891 | DOI:10.1186/s40246-026-00979-y
XPO1 inhibitor KPT-330 disrupts the core transcriptional regulatory circuitry of dedifferentiated liposarcoma by modulating the translation process
Oncogene, Published online: 16 April 2026; doi:10.1038/s41388-026-03794-w
XPO1 inhibitor KPT-330 disrupts the core transcriptional regulatory circuitry of dedifferentiated liposarcoma by modulating the translation processLLMs Judge Themselves: A Game-Theoretic Framework for Human-Aligned Evaluation
NED-Tree: Bridging the Semantic Gap with Nonlinear Element Decomposition Tree for LLM Nonlinear Optimization Modeling
Integrated spatial transcriptomics and pan-cancer XGBoost modeling uncover spatial drivers of immune exclusion and predict immunotherapy response
Cancer Immunol Immunother. 2026 Apr 2;75(4):131. doi: 10.1007/s00262-026-04374-3.
ABSTRACT
Immunotherapy has revolutionized cancer treatment, yet characterizing the spatial complexity of the tumor immune microenvironment remains a challenge. In this study, we established a comprehensive computational framework integrating multi-omics profiling across 27 cancer types to decode immune-related non-coding RNA regulatory networks. Moving beyond traditional bulk analysis, we utilized spatial transcriptomics to dissect the spatial localization of these regulators. We identified the SNHG6-BIRC5 axis as a critical driver of the "immune-cold" phenotype in lung adenocarcinoma. We provide visual evidence that this axis localizes to tumor nests and negatively correlates with T- cell infiltration, elucidating a mechanism of spatial immune exclusion. Validating the clinical relevance of these findings, genome-scale CRISPR-Cas9 screening data confirmed the functional essentiality of these targets for cancer cell survival. Furthermore, pharmacogenomic analysis revealed that high expression of this axis correlates with sensitivity to chemotherapy agents like Vinblastine, suggesting a potential stratification strategy for patients with immune-excluded tumors. To expand the clinical utility to immunotherapy prediction, we developed a pan-cancer XGBoost machine learning model incorporating 14 high-performance regulatory features. This model achieved robust performance in distinguishing immunotherapy responders from non-responders with an AUC of 0.771, outperforming traditional markers such as PD-L1. Collectively, this study highlights spatial determinants of immune exclusion and chemotherapy sensitivity- and presents a generalized machine- learning tool for precision immunotherapy stratification. The developed online resource is freely available to facilitate community-wide biomarker discovery.
PMID:41925746 | DOI:10.1007/s00262-026-04374-3