Normal view
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cs.AI, q-bio.NC updates on arXiv.org
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Distilling Image Prototypes for Guided Test-Time Adaptation
arXiv:2609.09737v1 Announce Type: cross Abstract: Test-Time Adaptation (TTA) enhances the robustness of models against distribution shifts but faces two critical challenges: error accumulation from noisy pseudo-labels and catastrophic forgetting of source knowledge. Uncertainty-based approaches designed to mitigate error accumulation often yield overconfident or computationally expensive estimates, while strategies intended to prevent forgetting via prototype replay rely on static representatio
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cs.AI, q-bio.NC updates on arXiv.org
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Rethinking Weak Supervision in Anomaly Detection: A Comprehensive Benchmark
arXiv:2605.26068v2 Announce Type: cross Abstract: Weakly supervised anomaly detection (WSAD) has developed in three primary directions: incomplete, inexact, and inaccurate supervision. However, these directions remain isolated, lacking a unified framework to assess whether they address unique challenges or share fundamental mechanics. This paper introduces WSADBench, the first benchmark that unifies evaluation across distinct weakly supervised scenarios, benchmarking diverse approaches from spe
Rethinking Weak Supervision in Anomaly Detection: A Comprehensive Benchmark
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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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cs.AI, q-bio.NC updates on arXiv.org
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LLMON: An LLM-native Markup Language to Leverage Structure and Semantics at the LLM Interface
arXiv:2603.22519v2 Announce Type: replace-cross Abstract: Textual Large Language Models (LLMs) provide a simple and familiar interface: a string of text is used for both input and output. However, the information conveyed to an LLM often has a richer structure and semantics, which is not conveyed in a string. For example, most prompts contain both instructions ("Summarize this paper into a paragraph") and data (the paper to summarize), but these are usually not distinguished when passed to the
LLMON: An LLM-native Markup Language to Leverage Structure and Semantics at the LLM Interface
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cs.AI, q-bio.NC updates on arXiv.org
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LLMON: An LLM-native Markup Language to Leverage Structure and Semantics at the LLM Interface
arXiv:2603.22519v1 Announce Type: cross Abstract: Textual Large Language Models (LLMs) provide a simple and familiar interface: a string of text is used for both input and output. However, the information conveyed to an LLM often has a richer structure and semantics, which is not conveyed in a string. For example, most prompts contain both instructions ("Summarize this paper into a paragraph") and data (the paper to summarize), but these are usually not distinguished when passed to the model. T
LLMON: An LLM-native Markup Language to Leverage Structure and Semantics at the LLM Interface
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Omics in Hepatocellular
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Multi-omics analysis and experimental validation uncovers prognosis significance of IKBIP in patients with hepatocellular carcinoma: a multicenter cohort study
BMC Gastroenterol. 2026 Mar 19. doi: 10.1186/s12876-026-04756-y. Online ahead of print.NO ABSTRACTPMID:41851828 | DOI:10.1186/s12876-026-04756-y
Multi-omics analysis and experimental validation uncovers prognosis significance of IKBIP in patients with hepatocellular carcinoma: a multicenter cohort study
BMC Gastroenterol. 2026 Mar 19. doi: 10.1186/s12876-026-04756-y. Online ahead of print.
NO ABSTRACT
PMID:41851828 | DOI:10.1186/s12876-026-04756-y