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cs.AI, q-bio.NC updates on arXiv.org
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Synergistic Vision-Language Reinforcement Enables Scalable On-Demand Analysis across Diverse Clinical Tasks
arXiv:2505.03380v2 Announce Type: replace-cross Abstract: Accurate delineation of tumors and surrounding organs-at-risk is essential for radiotherapy, surgery and treatment response assessment, yet remains time-consuming and expertise-intensive. Existing artificial intelligence systems often require manual spatial prompts or task-specific retraining, while generic class labels provide limited semantic grounding for heterogeneous disease targets. Here we present SyRe, a promptable segmentation f
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(Multiomics OR Omics) AND (Lung OR gastric OR Hepatocellular)
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Advances in Metabolic Reprogramming and Immune Regulatory Mechanisms in Lung Cancer
Oncol Res. 2026 Mar 23;34(4):11. doi: 10.32604/or.2026.076176. eCollection 2026.ABSTRACTLung cancer remains the leading cause of cancer-related mortality worldwide, primarily driven by metabolic reprogramming and immune evasion mechanisms within tumor cells. To adapt to the nutrient-deprived tumor microenvironment (TME), lung cancer cells undergo profound metabolic reprogramming, characterized by enhanced glycolysis (the Warburg effect), increased glutamine dependency (mediated by GLS1), and acc
Advances in Metabolic Reprogramming and Immune Regulatory Mechanisms in Lung Cancer
Oncol Res. 2026 Mar 23;34(4):11. doi: 10.32604/or.2026.076176. eCollection 2026.
ABSTRACT
Lung cancer remains the leading cause of cancer-related mortality worldwide, primarily driven by metabolic reprogramming and immune evasion mechanisms within tumor cells. To adapt to the nutrient-deprived tumor microenvironment (TME), lung cancer cells undergo profound metabolic reprogramming, characterized by enhanced glycolysis (the Warburg effect), increased glutamine dependency (mediated by GLS1), and accelerated lipid synthesis (involving enzymes such as FASN). These metabolic alterations not only remodel the TME but also dampen antitumor immune responses by promoting immunosuppressive cell populations (e.g., Tregs and M2 macrophages) and inhibiting effector functions of CD8+ T cells and natural killer (NK) cells. Critically, a bidirectional crosstalk operates between tumor cell metabolism and the immunosuppressive TME: metabolic reprogramming drives immune suppression through metabolite accumulation, whereas the immunosuppressive TME, in turn, promotes tumor cell adaptability-thus forming a positive feedback loop that reinforces immune evasion and therapy resistance. This review elucidates key molecular pathways governing metabolic reprogramming in lung cancer-spanning glucose, amino acid, and lipid metabolism-and their dynamic crosstalk with immune regulation, including epigenetic modifications and non-coding RNA-mediated mechanisms. Additionally, it evaluates emerging therapeutic strategies targeting the metabolic-immune axis, such as inhibitors of HK2 or GLS1 combined with anti-PD-1/PD-L1 agents, which aim to reverse immunosuppression and improve clinical outcomes. By synthesizing recent advances, this work provides a theoretical framework for precision oncology interventions, highlighting the potential of metabolic immunotherapies and future directions integrating AI and multi-omics data to overcome resistance in lung cancer.
PMID:41930159 | PMC:PMC13040304 | DOI:10.32604/or.2026.076176
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Omics In Lung
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Advances in Metabolic Reprogramming and Immune Regulatory Mechanisms in Lung Cancer
Oncol Res. 2026 Mar 23;34(4):11. doi: 10.32604/or.2026.076176. eCollection 2026.ABSTRACTLung cancer remains the leading cause of cancer-related mortality worldwide, primarily driven by metabolic reprogramming and immune evasion mechanisms within tumor cells. To adapt to the nutrient-deprived tumor microenvironment (TME), lung cancer cells undergo profound metabolic reprogramming, characterized by enhanced glycolysis (the Warburg effect), increased glutamine dependency (mediated by GLS1), and acc
Advances in Metabolic Reprogramming and Immune Regulatory Mechanisms in Lung Cancer
Oncol Res. 2026 Mar 23;34(4):11. doi: 10.32604/or.2026.076176. eCollection 2026.
ABSTRACT
Lung cancer remains the leading cause of cancer-related mortality worldwide, primarily driven by metabolic reprogramming and immune evasion mechanisms within tumor cells. To adapt to the nutrient-deprived tumor microenvironment (TME), lung cancer cells undergo profound metabolic reprogramming, characterized by enhanced glycolysis (the Warburg effect), increased glutamine dependency (mediated by GLS1), and accelerated lipid synthesis (involving enzymes such as FASN). These metabolic alterations not only remodel the TME but also dampen antitumor immune responses by promoting immunosuppressive cell populations (e.g., Tregs and M2 macrophages) and inhibiting effector functions of CD8+ T cells and natural killer (NK) cells. Critically, a bidirectional crosstalk operates between tumor cell metabolism and the immunosuppressive TME: metabolic reprogramming drives immune suppression through metabolite accumulation, whereas the immunosuppressive TME, in turn, promotes tumor cell adaptability-thus forming a positive feedback loop that reinforces immune evasion and therapy resistance. This review elucidates key molecular pathways governing metabolic reprogramming in lung cancer-spanning glucose, amino acid, and lipid metabolism-and their dynamic crosstalk with immune regulation, including epigenetic modifications and non-coding RNA-mediated mechanisms. Additionally, it evaluates emerging therapeutic strategies targeting the metabolic-immune axis, such as inhibitors of HK2 or GLS1 combined with anti-PD-1/PD-L1 agents, which aim to reverse immunosuppression and improve clinical outcomes. By synthesizing recent advances, this work provides a theoretical framework for precision oncology interventions, highlighting the potential of metabolic immunotherapies and future directions integrating AI and multi-omics data to overcome resistance in lung cancer.
PMID:41930159 | PMC:PMC13040304 | DOI:10.32604/or.2026.076176
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Nature Cancer
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PRET is a few-shot system for pan-cancer recognition without example training
Nature Cancer, Published online: 03 April 2026; doi:10.1038/s43018-026-01141-2Li et al. present PRET, a few-shot system for pan-cancer detection not requiring model fine-tuning, validated it in multicenter datasets and found that it outperformed existing approaches across tasks and pathologists in lymph node metastasis detection.
PRET is a few-shot system for pan-cancer recognition without example training
Nature Cancer, Published online: 03 April 2026; doi:10.1038/s43018-026-01141-2
Li et al. present PRET, a few-shot system for pan-cancer detection not requiring model fine-tuning, validated it in multicenter datasets and found that it outperformed existing approaches across tasks and pathologists in lymph node metastasis detection.-
cs.AI, q-bio.NC updates on arXiv.org
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Escaping the BLEU Trap: A Signal-Grounded Framework with Decoupled Semantic Guidance for EEG-to-Text Decoding
arXiv:2603.03312v1 Announce Type: cross Abstract: Decoding natural language from non-invasive EEG signals is a promising yet challenging task. However, current state-of-the-art models remain constrained by three fundamental limitations: Semantic Bias (mode collapse into generic templates), Signal Neglect (hallucination based on linguistic priors rather than neural inputs), and the BLEU Trap, where evaluation metrics are artificially inflated by high-frequency stopwords, masking a lack of true s
Escaping the BLEU Trap: A Signal-Grounded Framework with Decoupled Semantic Guidance for EEG-to-Text Decoding
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cs.AI, q-bio.NC updates on arXiv.org
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DenseMLLM: Standard Multimodal LLMs are Intrinsic Dense Predictors
arXiv:2602.14134v1 Announce Type: cross Abstract: Multimodal Large Language Models (MLLMs) have demonstrated exceptional capabilities in high-level visual understanding. However, extending these models to fine-grained dense prediction tasks, such as semantic segmentation and depth estimation, typically necessitates the incorporation of complex, task-specific decoders and other customizations. This architectural fragmentation increases model complexity and deviates from the generalist design of