Normal view
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cs.AI, q-bio.NC updates on arXiv.org
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Pelican-Sim 1.0: A General World Model Simulator for Embodied Intelligence
arXiv:2609.12036v1 Announce Type: cross Abstract: In this technical report, we propose Pelican-Sim 1.0, a general world model simulator for embodied intelligence that predicts future observations from visual context and robot actions to support downstream learning and decision making. The model incorporates four key design features: (1) Unified action representation: a 28-dimensional action value space covering most mainstream embodiments, keeping one model valid across heterogeneous devices. (
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cs.AI, q-bio.NC updates on arXiv.org
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Diffusion learning reveals viable parameter manifolds and compensation geometry in biological dynamical systems
arXiv:2607.03671v2 Announce Type: replace-cross Abstract: Models of complex systems often have many parameters, yet are constrained by far fewer experimentally accessible observables; consequently, similar activity can emerge from coordinated parameter changes. We formalize these compatible parameter sets as \emph{viable parameter manifolds}: the inverse images of target dynamical features under a parameter-to-feature map. The relevant codimension is not the number of reported features, but the
Diffusion learning reveals viable parameter manifolds and compensation geometry in biological dynamical systems
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Omics In Lung
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Advanced and underlying therapeutic strategies in transformed small cell lung cancer
Front Med (Lausanne). 2026 Aug 27;13:1865050. doi: 10.3389/fmed.2026.1865050. eCollection 2026.ABSTRACTTransformed small-cell lung cancer (T-SCLC) is a clinically important form of histologic transformation and a mechanism of acquired resistance in non-small-cell lung cancer (NSCLC). It is associated with poor prognosis, with a median overall survival of only about 9-13 months. This review summarizes recent advances in the mechanisms, diagnosis, monitoring, and treatment of T-SCLC. Repeat biopsy
Advanced and underlying therapeutic strategies in transformed small cell lung cancer
Front Med (Lausanne). 2026 Aug 27;13:1865050. doi: 10.3389/fmed.2026.1865050. eCollection 2026.
ABSTRACT
Transformed small-cell lung cancer (T-SCLC) is a clinically important form of histologic transformation and a mechanism of acquired resistance in non-small-cell lung cancer (NSCLC). It is associated with poor prognosis, with a median overall survival of only about 9-13 months. This review summarizes recent advances in the mechanisms, diagnosis, monitoring, and treatment of T-SCLC. Repeat biopsy remains the gold standard for confirming histologic transformation, whereas molecular profiling and liquid biopsy may facilitate early detection and longitudinal disease monitoring. Platinum-etoposide remains the most commonly used clinical standard after transformation, but its benefit is typically transient and durable disease control remains uncommon. Continuation of EGFR tyrosine kinase inhibitors combined with chemotherapy may prolong progression-free survival in selected patients but has not consistently improved overall survival. Anti-angiogenic therapy, particularly anlotinib, and chemo-immunotherapy have shown encouraging activity in selected patients, while emerging strategies targeting DLL3, MYC, SOX2, and epigenetic regulators may broaden the therapeutic landscape. Prospective studies integrating repeat tissue sampling, comprehensive genomic profiling, biomarker-guided patient stratification, pharmacogenomics, functional drug-sensitivity testing where feasible, and integrated multi-omics approaches are needed to advance molecularly guided and individualized treatment for T-SCLC.
PMID:42724635 | PMC:PMC13560167 | DOI:10.3389/fmed.2026.1865050
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(Multiomics OR Omics) AND (Lung OR gastric OR Hepatocellular)
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Advanced and underlying therapeutic strategies in transformed small cell lung cancer
Front Med (Lausanne). 2026 Aug 27;13:1865050. doi: 10.3389/fmed.2026.1865050. eCollection 2026.ABSTRACTTransformed small-cell lung cancer (T-SCLC) is a clinically important form of histologic transformation and a mechanism of acquired resistance in non-small-cell lung cancer (NSCLC). It is associated with poor prognosis, with a median overall survival of only about 9-13 months. This review summarizes recent advances in the mechanisms, diagnosis, monitoring, and treatment of T-SCLC. Repeat biopsy
Advanced and underlying therapeutic strategies in transformed small cell lung cancer
Front Med (Lausanne). 2026 Aug 27;13:1865050. doi: 10.3389/fmed.2026.1865050. eCollection 2026.
ABSTRACT
Transformed small-cell lung cancer (T-SCLC) is a clinically important form of histologic transformation and a mechanism of acquired resistance in non-small-cell lung cancer (NSCLC). It is associated with poor prognosis, with a median overall survival of only about 9-13 months. This review summarizes recent advances in the mechanisms, diagnosis, monitoring, and treatment of T-SCLC. Repeat biopsy remains the gold standard for confirming histologic transformation, whereas molecular profiling and liquid biopsy may facilitate early detection and longitudinal disease monitoring. Platinum-etoposide remains the most commonly used clinical standard after transformation, but its benefit is typically transient and durable disease control remains uncommon. Continuation of EGFR tyrosine kinase inhibitors combined with chemotherapy may prolong progression-free survival in selected patients but has not consistently improved overall survival. Anti-angiogenic therapy, particularly anlotinib, and chemo-immunotherapy have shown encouraging activity in selected patients, while emerging strategies targeting DLL3, MYC, SOX2, and epigenetic regulators may broaden the therapeutic landscape. Prospective studies integrating repeat tissue sampling, comprehensive genomic profiling, biomarker-guided patient stratification, pharmacogenomics, functional drug-sensitivity testing where feasible, and integrated multi-omics approaches are needed to advance molecularly guided and individualized treatment for T-SCLC.
PMID:42724635 | PMC:PMC13560167 | DOI:10.3389/fmed.2026.1865050
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Nature - Issue - nature.com science feeds
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Sideline vested interests to reform China’s research
Nature, Published online: 08 September 2026; doi:10.1038/d41586-026-02797-7Sideline vested interests to reform China’s research
Sideline vested interests to reform China’s research
Nature, Published online: 08 September 2026; doi:10.1038/d41586-026-02797-7
Sideline vested interests to reform China’s research-
Omics In Lung
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Local lactate-driven H3K18 lactylation impairs anti-influenza immunity through NRF2-dependent dendritic cell dysfunction
Cell Rep. 2026 Sep 3;45(9):117943. doi: 10.1016/j.celrep.2026.117943. Online ahead of print.ABSTRACTMetabolic alterations are increasingly recognized during influenza virus infection, but how local lactate accumulation shapes antiviral immunity remains poorly characterized. By integrating time-series targeted energy metabolomics, single-cell RNA sequencing, flow cytometry, and functional perturbation, we show that influenza virus infection preferentially increases lactate within the lung microen
Local lactate-driven H3K18 lactylation impairs anti-influenza immunity through NRF2-dependent dendritic cell dysfunction
Cell Rep. 2026 Sep 3;45(9):117943. doi: 10.1016/j.celrep.2026.117943. Online ahead of print.
ABSTRACT
Metabolic alterations are increasingly recognized during influenza virus infection, but how local lactate accumulation shapes antiviral immunity remains poorly characterized. By integrating time-series targeted energy metabolomics, single-cell RNA sequencing, flow cytometry, and functional perturbation, we show that influenza virus infection preferentially increases lactate within the lung microenvironment, where it restrains pulmonary CD8+ T cell response. Mechanistically, extracellular lactate enters dendritic cells through monocarboxylate transporter (MCT)-dependent transport and induces a tolerogenic-like state marked by impaired maturation, reduced costimulation, and diminished CD8+ T cell-priming capacity. Direct experimental evidence identifies H3K18la as a prominent lactate-responsive histone lactylation mark, while multi-omics integration links it to enhancer accessibility and NRF2 pathway activation. Functional studies further show that NRF2 promotes dendritic cell suppression by reinforcing tolerogenic programs and limiting mtROS-dependent XBP1 splicing. Together, these findings reveal a lactate-driven histone lactylation-NRF2 pathway that modulates antiviral immunity during influenza infection.
PMID:42690934 | DOI:10.1016/j.celrep.2026.117943
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Omics in Hepatocellular
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Integrated single-cell multi-omics characterization reveals lipid-associated macrophage-mediated immunosuppression in neoadjuvant immunotherapy of hepatocellular carcinoma
Nat Commun. 2026 Jul 31;17(1):9381. doi: 10.1038/s41467-026-75949-y.ABSTRACTHepatocellular carcinoma (HCC) is a cancer with high incidence and mortality rate. Although immune checkpoint inhibitors (ICIs) improved survival outcomes for HCC patients, limited objective response rate highlights the urgency of investigating determinants of immunotherapy. Here, we explore HCC resistance mechanisms following neoadjuvant αPD-1 immunotherapy by constructing a comprehensive multi-modal single-cell transcr
Integrated single-cell multi-omics characterization reveals lipid-associated macrophage-mediated immunosuppression in neoadjuvant immunotherapy of hepatocellular carcinoma
Nat Commun. 2026 Jul 31;17(1):9381. doi: 10.1038/s41467-026-75949-y.
ABSTRACT
Hepatocellular carcinoma (HCC) is a cancer with high incidence and mortality rate. Although immune checkpoint inhibitors (ICIs) improved survival outcomes for HCC patients, limited objective response rate highlights the urgency of investigating determinants of immunotherapy. Here, we explore HCC resistance mechanisms following neoadjuvant αPD-1 immunotherapy by constructing a comprehensive multi-modal single-cell transcriptomic atlas consisting of 14 HCC patients treated with αPD-1 from our cohort (ClinicalTrials.gov ID: NCT06571396) and 60 external HCC cases with heterogeneous treatment backgrounds. Supervised by clinical outcomes of our cohort, we identify positive and negative regulators of immunotherapy within the tumor immune microenvironment (TIME), especially lipid-associated macrophages (LAM) with increased lipid metabolic state in non-responders and characterized by C1QA, FABP1, and APOA1 expression. We further show the presence, exogenous inducements and immunosuppressive functions of LAM, along with regulation strategies of its lipid-associated condition, including lycopene and chiglitazar. Furthermore, we construct interaction networks of immune regulators across responders and non-responders, showing distinct ligand-receptor landscapes with intervention targets. We reveal the TIME components including immunosuppressive LAMs that influence immunotherapy outcomes, thus providing evidence and insights for exploring immune landscape and therapeutic strategies for HCC immunotherapy. ClinicalTrials.gov ID: NCT06571396.
PMID:42680737 | PMC:PMC13534469 | DOI:10.1038/s41467-026-75949-y
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Nature - Issue - nature.com science feeds
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EBV strain interacts with host HLA to drive nasopharyngeal carcinoma risk
Nature, Published online: 15 April 2026; doi:10.1038/s41586-026-10416-8A genome-to-genome association study identifies host and viral risk factors that interact to drive nasopharyngeal carcinoma endemicity in southern China.
EBV strain interacts with host HLA to drive nasopharyngeal carcinoma risk
Nature, Published online: 15 April 2026; doi:10.1038/s41586-026-10416-8
A genome-to-genome association study identifies host and viral risk factors that interact to drive nasopharyngeal carcinoma endemicity in southern China.-
Nature - Issue - nature.com science feeds
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DNA damage drives antigen diversification in <i>Trypanosoma brucei</i>
Nature, Published online: 08 April 2026; doi:10.1038/s41586-026-10337-6An in vitro toolkit for studying VSG diversification defines key molecular requirements underlying the formation of mosaic VSGs, providing an experimental framework for the exploration of antigen diversification in Trypanosoma brucei and in other pathogenic microorganisms.
DNA damage drives antigen diversification in <i>Trypanosoma brucei</i>
Nature, Published online: 08 April 2026; doi:10.1038/s41586-026-10337-6
An in vitro toolkit for studying VSG diversification defines key molecular requirements underlying the formation of mosaic VSGs, providing an experimental framework for the exploration of antigen diversification in Trypanosoma brucei and in other pathogenic microorganisms.-
cs.AI, q-bio.NC updates on arXiv.org
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Fine-grained Analysis of Stability and Generalization for Stochastic Bilevel Optimization
arXiv:2604.04090v1 Announce Type: cross Abstract: Stochastic bilevel optimization (SBO) has been integrated into many machine learning paradigms recently, including hyperparameter optimization, meta learning, and reinforcement learning. Along with the wide range of applications, there have been numerous studies on the computational behavior of SBO. However, the generalization guarantees of SBO methods are far less understood from the lens of statistical learning theory. In this paper, we provid
Fine-grained Analysis of Stability and Generalization for Stochastic Bilevel Optimization
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cs.AI, q-bio.NC updates on arXiv.org
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Contextual Distributionally Robust Optimization with Causal and Continuous Structure: An Interpretable and Tractable Approach
arXiv:2601.11016v2 Announce Type: replace-cross Abstract: In this paper, we introduce a framework for contextual distributionally robust optimization (DRO) that considers the causal and continuous structure of the underlying distribution by developing interpretable and tractable decision rules that prescribe decisions using covariates. We first introduce the causal Sinkhorn discrepancy (CSD), an entropy-regularized causal Wasserstein distance that encourages continuous transport plans while pre
Contextual Distributionally Robust Optimization with Causal and Continuous Structure: An Interpretable and Tractable Approach
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Oncogene - Issue - nature.com science feeds
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Strand-asymmetric G-runs and G4s downstream of TSS modulate tumor suppressor gene transcription
Oncogene, Published online: 02 April 2026; doi:10.1038/s41388-026-03761-5Strand-asymmetric G-runs and G4s downstream of TSS modulate tumor suppressor gene transcription
Strand-asymmetric G-runs and G4s downstream of TSS modulate tumor suppressor gene transcription
Oncogene, Published online: 02 April 2026; doi:10.1038/s41388-026-03761-5
Strand-asymmetric G-runs and G4s downstream of TSS modulate tumor suppressor gene transcription-
cs.AI, q-bio.NC updates on arXiv.org
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ASI-Evolve: AI Accelerates AI
arXiv:2603.29640v1 Announce Type: new Abstract: Can AI accelerate the development of AI itself? While recent agentic systems have shown strong performance on well-scoped tasks with rapid feedback, it remains unclear whether they can tackle the costly, long-horizon, and weakly supervised research loops that drive real AI progress. We present ASI-Evolve, an agentic framework for AI-for-AI research that closes this loop through a learn-design-experiment-analyze cycle. ASI-Evolve augments standard
ASI-Evolve: AI Accelerates AI
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Oncogene - Issue - nature.com science feeds
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Targeting FTO shows therapeutic potential in esophageal squamous cell carcinoma by modulating microRNA biogenesis
Oncogene, Published online: 01 April 2026; doi:10.1038/s41388-026-03754-4Targeting FTO shows therapeutic potential in esophageal squamous cell carcinoma by modulating microRNA biogenesis
Targeting FTO shows therapeutic potential in esophageal squamous cell carcinoma by modulating microRNA biogenesis
Oncogene, Published online: 01 April 2026; doi:10.1038/s41388-026-03754-4
Targeting FTO shows therapeutic potential in esophageal squamous cell carcinoma by modulating microRNA biogenesis-
cs.AI, q-bio.NC updates on arXiv.org
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CyberGym: Evaluating AI Agents' Real-World Cybersecurity Capabilities at Scale
arXiv:2506.02548v3 Announce Type: replace-cross Abstract: AI agents have significant potential to reshape cybersecurity, making a thorough assessment of their capabilities critical. However, existing evaluations fall short, because they are based on small-scale benchmarks and only measure static outcomes, failing to capture the full, dynamic range of real-world security challenges. To address these limitations, we introduce CyberGym, a large-scale benchmark featuring 1,507 real-world vulnerabil
CyberGym: Evaluating AI Agents' Real-World Cybersecurity Capabilities at Scale
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cs.AI, q-bio.NC updates on arXiv.org
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From Noisy Labels to Intrinsic Structure: A Geometric-Structural Dual-Guided Framework for Noise-Robust Medical Image Segmentation
arXiv:2509.02419v2 Announce Type: replace-cross Abstract: The effectiveness of convolutional neural networks in medical image segmentation relies on large-scale, high-quality annotations, which are costly and time-consuming to obtain. Even expert-labeled datasets inevitably contain noise arising from subjectivity and coarse delineations, which disrupt feature learning and adversely impact model performance. To address these challenges, this study propose a Geometric-Structural Dual-Guided Netwo
From Noisy Labels to Intrinsic Structure: A Geometric-Structural Dual-Guided Framework for Noise-Robust Medical Image Segmentation
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(Multiomics OR Omics) AND (Lung OR gastric OR Hepatocellular)
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NUP85 as a Pan-Cancer Immune Biomarker: Integrated Multi Omics and Functional Analyses Reveal Its Role in Tumor Prognosis
Immunotargets Ther. 2026 Mar 17;15:541852. doi: 10.2147/ITT.S541852. eCollection 2026.ABSTRACTPURPOSE: NUP85 encodes protein components of the Nup107-160 subunit of the nuclear pore complex, belonging to the Nucleoporins (NUPs) family, potentially implicating its role in human cancer. This study aims to elucidate the potential involvement of NUP85 in cancer pathogenesis.METHODS: Leveraging data from The Cancer Genome Atlas (TCGA), Genotype-Tissue Expression (GTEx), Clinical Proteomic Tumor Analy
NUP85 as a Pan-Cancer Immune Biomarker: Integrated Multi Omics and Functional Analyses Reveal Its Role in Tumor Prognosis
Immunotargets Ther. 2026 Mar 17;15:541852. doi: 10.2147/ITT.S541852. eCollection 2026.
ABSTRACT
PURPOSE: NUP85 encodes protein components of the Nup107-160 subunit of the nuclear pore complex, belonging to the Nucleoporins (NUPs) family, potentially implicating its role in human cancer. This study aims to elucidate the potential involvement of NUP85 in cancer pathogenesis.
METHODS: Leveraging data from The Cancer Genome Atlas (TCGA), Genotype-Tissue Expression (GTEx), Clinical Proteomic Tumor Analysis Consortium (CPTAC), Cancer Cell Line Encyclopedia (CCLE), Human Protein Atlas (HPA), Gene Expression Profiling Interactive Analysis (GEPIA), CellMiner, and GeneMANIA databases, we investigated the role of NUP85 across various tumors. Correlations between NUP85 expression and pathological stage, histological grade, survival, immune infiltration, tumor mutational burden (TMB), microsatellite instability (MSI), drug resistance, DNA methylation, copy number variation (CNV), and single-cell expression were analyzed. Gene functional enrichment analysis was conducted to explore NUP85-associated pathways. Molecular biology experiments including Western blotting, flow cytometry, trans-well migration, and invasion assays were performed to validate NUP85's oncogenic role in lung adenocarcinoma (LUAD) and oral squamous cell carcinoma (OSCC) cell lines.
RESULTS: Our findings reveal up-regulated expression of NUP85 in most tumor tissues, with significant correlations observed with pathological stage, survival, immune infiltration, TMB, MSI, drug resistance, DNA methylation, and CNV. Molecular biology experiments confirm NUP85's tumor-promoting role in LUAD and OSCC cell lines. Single-cell sequencing data suggest elevated NUP85 expression primarily in proliferative T cells (Tprolif).
CONCLUSION: NUP85 emerges as a potential tumor marker associated with tumor immunity and poor prognosis. These insights offer avenues for the development of novel therapeutic targets and anti-neoplastic drugs.
PMID:41869435 | PMC:PMC13005628 | DOI:10.2147/ITT.S541852
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Omics in Hepatocellular
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Hypoxia-related and immune phenotype-related fusion model for non-invasive prognostication of hepatocellular carcinoma treated by TACE: a multicentre study
Gut. 2026 Mar 30:gutjnl-2025-337938. doi: 10.1136/gutjnl-2025-337938. Online ahead of print.ABSTRACTBACKGROUND: Survival outcomes after transarterial chemoembolisation (TACE) vary in hepatocellular carcinoma (HCC) patients, and existing prognostic scores and imaging models often lack generalisability and biological interpretability.OBJECTIVE: To develop and validate a multimodal prognostication model for HCC that allows for a precise assessment of survival outcomes of HCC patients receiving TACE
Hypoxia-related and immune phenotype-related fusion model for non-invasive prognostication of hepatocellular carcinoma treated by TACE: a multicentre study
Gut. 2026 Mar 30:gutjnl-2025-337938. doi: 10.1136/gutjnl-2025-337938. Online ahead of print.
ABSTRACT
BACKGROUND: Survival outcomes after transarterial chemoembolisation (TACE) vary in hepatocellular carcinoma (HCC) patients, and existing prognostic scores and imaging models often lack generalisability and biological interpretability.
OBJECTIVE: To develop and validate a multimodal prognostication model for HCC that allows for a precise assessment of survival outcomes of HCC patients receiving TACE therapy.
DESIGN: This study enrolled 1448 HCC patients, including a TACE cohort (n=1349), a biomarker subset from a randomised trial (n=41), a single-cell RNA sequencing cohort and The Cancer Genome Atlas (TCGA) HCC cohort (n=50). Pre-treatment contrast-enhanced CT images were used to construct deep learning and conventional radiomic models. The early-fusion and late-fusion models (LFMs) were compared, and a clinical-radiologic model (CRM) was formed by integrating the better-performing LFM with clinical variables. Using TCGA data and single-cell transcriptomic profiles, the differences between high-score and low-score groups in tumour immune microenvironment, cellular functional states and key signalling pathways were investigated.
RESULTS: The CRM effectively stratified patients' survival across multiple independent cohorts and achieved more granular risk stratification than the existing clinical models. Multi-omic analyses revealed that in the LFM high-score group, myelocytomatosis oncogene was activated, epithelial-mesenchymal transition enhanced, glycolysis upregulated and hypoxia pathway activated. Single-cell transcriptomic data confirmed that virtually all cell types in high-risk patients scored high in hypoxia, and cytotoxic T cells had a reduced cytotoxic activity.
CONCLUSION: The CRM model can non-invasively predict the prognosis of HCC patients treated by TACE therapy.
PMID:41856522 | DOI:10.1136/gutjnl-2025-337938
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Cell
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β-hydroxybutyrate enhances the metabolic fitness of CAR T cells in cancer
β-hydroxybutyrate (BHB), the ketone body associated with a ketogenic diet, metabolically reprograms and fuels CAR T cells to achieve proliferation, cytokine production, and superior tumor control. These findings suggest that BHB supplementation may be a practical way to boost adoptive cancer immunotherapy.
β-hydroxybutyrate enhances the metabolic fitness of CAR T cells in cancer
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cs.AI, q-bio.NC updates on arXiv.org
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ARL-Tangram: Unleash the Resource Efficiency in Agentic Reinforcement Learning
arXiv:2603.13019v1 Announce Type: cross Abstract: Agentic reinforcement learning (RL) has emerged as a transformative workload in cloud clusters, enabling large language models (LLMs) to solve complex problems through interactions with real world. However, unlike traditional RL, agentic RL demands substantial external cloud resources, e.g., CPUs for code execution and GPUs for reward models, that exist outside the primary training cluster. Existing agentic RL framework typically rely on static