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Normal view

Received — 27 May 2026 ⏭

A Non-Canonical Role of SMAD4 in Regulating 3D Genome Architecture to Inhibit Lung Squamous Cell Carcinoma Development

✇(Multiomics OR Omics) AND (Lung OR gastric OR Hepatocellular)
By: Qian Tang · Chen Lian · Xinyan Han · Xuhan Zhang · Zihan Wang · Boyu Wang · Taoyu Zhu · Xinrui Lin · Xiaolei Wang · Yaping Xu · Manyu Xiao · Zijin Wang · Junming Li · Silin Chen · Yunze Wang · Yufei Liu · Songsong Li · Zuolin Shen · Xi Lu · Xueqi Han · Yilu Zhou · Mingyang Xiao · Jiayi Ran · Xiaoran Cao · Xinyi Xu · Hugo Sámano-Sánchez · Alfredo Rodríguez · Lian Wang · Shuifang Chen · Zhanyu Xu · Shirong Zhang · Nuo Yang · Yong Tang · Jian Liu
26 May 2026 at 18:00

Adv Sci (Weinh). 2026 May 26:e75839. doi: 10.1002/advs.75839. Online ahead of print.

ABSTRACT

Lung squamous cell carcinoma (LUSC) lacks clearly defined key drivers and effective targeted therapies, reflecting an incomplete understanding of its molecular pathogenesis. Here, we identify SMAD4 as a critical regulator of three-dimensional (3D) genome organization in LUSC and uncover a mechanistic link between tumor suppressor loss and oncogenic transcriptional activation. By integrating clinical datasets, genetically engineered mouse models, human and murine LUSC cell lines, and multi-omics analyses, we demonstrate that SMAD4 deficiency promotes LUSC progression by unleashing EP300-mediated enhancer-promoter looping at the SOX2 locus. Mechanistically, SMAD4 does not directly bind SOX2 regulatory elements but instead constrains chromatin looping by sequestering EP300 away from loop anchor regions. Loss of SMAD4 leads to enhanced H3K27ac deposition, aberrant SOX2 activation, and increased LUSC tumor cell proliferation. Together, these findings reveal a non-canonical role for a transcription factor (e.g., SMAD4) in regulating dysregulated 3D genome architecture to inhibit tumor development.

PMID:42189071 | DOI:10.1002/advs.75839

A Non-Canonical Role of SMAD4 in Regulating 3D Genome Architecture to Inhibit Lung Squamous Cell Carcinoma Development

✇Omics In Lung
By: Qian Tang · Chen Lian · Xinyan Han · Xuhan Zhang · Zihan Wang · Boyu Wang · Taoyu Zhu · Xinrui Lin · Xiaolei Wang · Yaping Xu · Manyu Xiao · Zijin Wang · Junming Li · Silin Chen · Yunze Wang · Yufei Liu · Songsong Li · Zuolin Shen · Xi Lu · Xueqi Han · Yilu Zhou · Mingyang Xiao · Jiayi Ran · Xiaoran Cao · Xinyi Xu · Hugo Sámano-Sánchez · Alfredo Rodríguez · Lian Wang · Shuifang Chen · Zhanyu Xu · Shirong Zhang · Nuo Yang · Yong Tang · Jian Liu
26 May 2026 at 18:00

Adv Sci (Weinh). 2026 May 26:e75839. doi: 10.1002/advs.75839. Online ahead of print.

ABSTRACT

Lung squamous cell carcinoma (LUSC) lacks clearly defined key drivers and effective targeted therapies, reflecting an incomplete understanding of its molecular pathogenesis. Here, we identify SMAD4 as a critical regulator of three-dimensional (3D) genome organization in LUSC and uncover a mechanistic link between tumor suppressor loss and oncogenic transcriptional activation. By integrating clinical datasets, genetically engineered mouse models, human and murine LUSC cell lines, and multi-omics analyses, we demonstrate that SMAD4 deficiency promotes LUSC progression by unleashing EP300-mediated enhancer-promoter looping at the SOX2 locus. Mechanistically, SMAD4 does not directly bind SOX2 regulatory elements but instead constrains chromatin looping by sequestering EP300 away from loop anchor regions. Loss of SMAD4 leads to enhanced H3K27ac deposition, aberrant SOX2 activation, and increased LUSC tumor cell proliferation. Together, these findings reveal a non-canonical role for a transcription factor (e.g., SMAD4) in regulating dysregulated 3D genome architecture to inhibit tumor development.

PMID:42189071 | DOI:10.1002/advs.75839

DRIVE: Modeling Skills at the Reasoning and Interaction Levels for Web Agents under Continual Learning

✇cs.AI, q-bio.NC updates on arXiv.org
By: Xirui Liu · Sihang Zhou · Yanning Hou · Rong Zhou · Haoyuan Chen · Maolin He · Siwei Wang · Hao Chen · Jian Huang
26 May 2026 at 12:00
arXiv:2605.23939v1 Announce Type: new Abstract: Web agents require both high-level reasoning (for task decomposition) and low-level interactions (for page elements manipulation) to conduct different tasks. However, these knowledge types differ fundamentally: reasoning knowledge (e.g., booking a flight requires first searching for routes) is abstract and transferable across websites, while interaction knowledge (e.g., clicking the Search button at a specific coordinate on Site A) depends heavily on page-specific contexts. Existing methods store experiences uniformly. This creates a dilemma: abstract representations lose executability on concrete pages, while concrete representations fail to generalize across domains. This entanglement limits capability accumulation: on new websites, agents either fail to recognize reusable task logic due to surface-level differences or attempt infeasible actions from outdated page structures. To disentangle them, we propose DRIVE, a dual-level skill modeling framework separating historical experience into natural language reasoning skills, which capture transferable task logic, and programmatic interaction skills, grounding abstract actions to executable operations. A scene-aware coordination mechanism adaptively retrieves and invokes these dual-level skills based on task semantics. DRIVE also uses skill-level reflection to identify hierarchy-specific failure modes, enabling targeted skill library expansion and refinement. Experiments across five WebArena domains show DRIVE attains an average task success rate of 52.8%, exceeding the skill-free baseline by 7.3 percentage points. Further ablations show reasoning and interaction skills provide distinct, complementary benefits, supporting separation of transferable task logic from executable page-level operations.

GlobalDentBench: A Multinational Benchmark for Evaluating LLM Clinical Reasoning in Dentistry with Expert Calibration

✇cs.AI, q-bio.NC updates on arXiv.org
By: Junjie Zhao · Jingyi Liang · Zhenyang Cai · Jiaming Zhang · Zhenwei Wen · Shuzhi Deng · Wenjing Yi · Chunfeng Luo · Hexian Zhang · Junying Chen · Tianrui Liu · Zhuhui Bai · Zixu Zhang · Pradeep Singh · Xiang Liu · Jianquan Li · Nhan L Tran · Falk Schwendicke · Zuolin Jin · Lijian Jin · Liangyi Chen · Wei-fa Yang · Benyou Wang · Junwen Wang · Shan Jiang
26 May 2026 at 12:00
arXiv:2605.24636v2 Announce Type: new Abstract: While large language models (LLMs) hold transformative potential for medicine, their reasoning robustness and safety in real-world clinical scenarios remain critically underexplored, particularly in dentistry. Here we introduce GlobalDentBench, the first multinational dental benchmark, featuring a taxonomy that encompasses 14 dental specialties across 88 countries and regions spanning six continents. The benchmark comprises 8,978 expert-validated questions across three formats (multiple-choice, short-answer, and case-based questions) and assesses three progressive reasoning levels: knowledge recall (L1), routine reasoning (L2), and individualized reasoning (L3). To ensure data quality, the automated construction framework was calibrated by six senior dentists, achieving expert agreement rates of 99.98% for multiple-choice and short-answer questions and 96.78% for the more complex case-based questions. Evaluation of 12 frontier LLMs on GlobalDentBench revealed a sharp, stepwise performance degradation with increasing reasoning complexity. Specifically, accuracy plummeted from 81.34% on multiple-choice to 64.53% on short-answer and 22.34% on case-based questions, while declining markedly from 74.01% at L1 to 55.64% at L2 and 35.71% at L3. More critically, risk analysis of real-world dental cases demonstrated an alarming overall unsafe rate of 31.01% in LLM-generated clinical recommendations, with 4.51% posing risks of irreversible patient harm and risks particularly pronounced in specialties such as orthodontics. These findings expose fundamental limitations in the medical reasoning and safety of current LLMs. Consequently, GlobalDentBench provides a scalable foundation for trustworthy clinical AI evaluation, underscoring the urgent need for rigorous validation before the safe deployment of these models in healthcare.

Towards Multi-Turn Dialog Systems for Industrial Asset Operations and Maintenance

✇cs.AI, q-bio.NC updates on arXiv.org
By: Chengrui Li · Rujing Li · Yitong Bai · Rui Li
26 May 2026 at 12:00
arXiv:2605.24953v1 Announce Type: new Abstract: Industrial asset operations and maintenance question answering is inherently multi-turn, iterative, and highly dependent on external tool invocation. However, the conventional plan-execute single-agent architecture exhibits clear limitations in maintaining cross-turn context, and reusing intermediate results. In this paper, we present a multi-turn dialog system designed for industrial scenarios based on a supervisor-specialist multi-agent architecture. To alleviate tool invocation bottlenecks, the system incorporates structured artifact reuse, dynamic replanning, and parallel tool execution. Evaluation results show that our system achieves better response quality compared with the baseline, with planning effectiveness increasing by 54.5% and task completion improving by 37.8%. System profiling further shows that cross-turn artifact reuse effectively reduces redundant tool invocation, decreasing the tool-time share from 47.3% to 26.3% and making turns 2-5 approximately 4.2x faster than the first turn.

FrontierOR: Benchmarking LLMs' Capacity for Efficient Algorithm Design in Large-Scale Optimization

✇cs.AI, q-bio.NC updates on arXiv.org
By: Minwei Kong · Chonghe Jiang · Ao Qu · Wenbin Ouyang · Zhaoming Zeng · Xiaotong Guo · Zhekai Li · Junyi Li · Yi Fan · Xinshou Zheng · Xi Jing · Yikai Zhang · Zhiwei Liang · Seonghoo Kim · Runqing Yang · Zijian Zhou · Sirui Li · Han Zheng · Wangyang Ying · Ou Zheng · Chonghuan Wang · Jinglong Zhao · Hanzhang Qin · Cathy Wu · Paul Pu Liang · Jinhua Zhao · Hai Wang
26 May 2026 at 12:00
arXiv:2605.25246v2 Announce Type: new Abstract: Large language models (LLMs) are increasingly used for optimization modeling and solver-code generation, yet practical operations research and optimization problems often require a harder capability: designing scalable algorithms that exploit problem structure and outperform direct formulation-and-solve baselines. Existing benchmarks are limited to small or simplified examples far below real-world scale and complexity. We introduce FrontierOR, among the first benchmarks to systematically evaluate LLM-based efficient algorithm design for realistic large-scale optimization problems. FrontierOR includes 180 tasks derived from methodologically diverse papers published in top-tier operations research venues, each with standardized instances and a hidden, expert-verified evaluation suite. We evaluate seven LLMs spanning frontier, cost-effective, and open-source models both in one-shot and test-time evolution settings. The results reveal that frontier models still struggle to move from executable formulations to efficient optimization algorithms: the strongest one-shot model outperforms Gurobi in only 31% of cases in both solution quality and computational efficiency, and even strong coding agents with test-time evolution achieve only 50% on selected hard tasks. FrontierOR establishes a practical evaluation platform for LLM-based optimization algorithm design, which enables future LLMs and agents to be systematically tested on whether they can move beyond correct formulation toward a feasible, high-quality, and efficient algorithm.

AutoResearchClaw: Self-Reinforcing Autonomous Research with Human-AI Collaboration

✇cs.AI, q-bio.NC updates on arXiv.org
By: Jiaqi Liu · Shi Qiu · Mairui Li · Bingzhou Li · Haonian Ji · Siwei Han · Xinyu Ye · Peng Xia · Zihan Dong · Meng Chen · Congyu Zhang · Letian Zhang · Guiming Chen · Haoqin Tu · Xinyu Yang · Lu Feng · Xujiang Zhao · Haifeng Chen · Jiawei Zhou · Xiao Wang · Weitong Zhang · Hongtu Zhu · Yun Li · Jieru Mei · Hongliang Fei · Jiaheng Zhang · Linjie Li · Linjun Zhang · Yuyin Zhou · Sheng Wang · Caiming Xiong · James Zou · Zeyu Zheng · Cihang Xie · Mingyu Ding · Huaxiu Yao
26 May 2026 at 12:00
arXiv:2605.20025v2 Announce Type: replace Abstract: Automating scientific discovery requires more than generating papers from ideas. Real research is iterative: hypotheses are challenged from multiple perspectives, experiments fail and inform the next attempt, and lessons accumulate across cycles. Existing autonomous research systems often model this process as a linear pipeline: they rely on single-agent reasoning, stop when execution fails, and do not carry experience across runs. We present AutoResearchClaw, a multi-agent autonomous research pipeline built on five mechanisms: structured multi-agent debate for hypothesis generation and result analysis, a self-healing executor with a \textsc{Pivot}/\textsc{Refine} decision loop that transforms failures into information, verifiable result reporting that prevents fabricated numbers and hallucinated citations, human-in-the-loop collaboration with seven intervention modes spanning full autonomy to step-by-step oversight, and cross-run evolution that converts past mistakes into future safeguards. On ARC-Bench, a 25-topic experiment-stage benchmark, AutoResearchClaw outperforms AI Scientist v2 by 54.7%. A human-in-the-loop ablation across seven intervention modes reveals that precise, targeted collaboration at high-leverage decision points consistently outperforms both full autonomy and exhaustive step-by-step oversight. We position AutoResearchClaw as a research amplifier that augments rather than replaces human scientific judgment. Code is available at https://github.com/aiming-lab/AutoResearchClaw.

Ferroptosis and macrophage polarization: mechanisms, interplay, and implications for medical applications

✇Cell Death Discovery nature.com science feeds
By: Yajuan Zhao · Jianbin Fu · Ping Zhao · Yuan Jiang · Yuhan Wang · Yaopeng Zhang · Zhaorui Li · Yongjun Zhao · Niannian Li · Bao Lang · Yanhua Luo
23 May 2026 at 08:00

Cell Death Discovery, Published online: 23 May 2026; doi:10.1038/s41420-026-03147-2

Ferroptosis and macrophage polarization: mechanisms, interplay, and implications for medical applications

PRXL2B facilitates the progression of hepatocellular carcinoma and the therapeutic efficacy of oncolytic adenovirus H101 through the PI3K/AKT/PD-L1 axis

✇Omics in Hepatocellular
By: Ziqi Zhang · Hongli Chen · Yangming Liu · Hao Wang · You Yan · Yanxi Yu · Zuotian Huang · Yanyao Liu · Wei Li · Zhongjun Wu · Meiqing Kang · Xiaoyong Luo · Ping Che · Rui Liao
20 May 2026 at 18:00

Biosci Trends. 2026 May 21. doi: 10.5582/bst.2026.01000. Online ahead of print.

ABSTRACT

Oncolytic adenovirus H101 has shown antitumor activity in hepatocellular carcinoma (HCC), but the molecular determinants of treatment response remain unclear. In this study, a Hepa1-6 subcutaneous tumor model was established in C57BL/6 mice and treated with intratumoral H101, followed by integrated transcriptomic and proteomic analyses to identify candidate genes associated with H101 response. PRXL2B was selected for further investigation using public multi-omics datasets, tissue microarray-based immunohistochemistry, in vitro functional assays, mechanistic analyses, and in vivo validation experiments. Integrated multi-omics analyses identified PRXL2B as a candidate gene downregulated after H101 treatment. Public datasets and tissue-based validation further showed that PRXL2B was upregulated in HCC tissues. In MHCC97H and HCCLM3 cells, PRXL2B knockdown inhibited proliferation, migration, and invasion, promoted apoptosis and cell-cycle arrest, and enhanced the antitumor effect of H101. Mechanistically, PRXL2B silencing reduced AKT phosphorylation and PD-L1 expression. In vivo, PRXL2B knockdown suppressed tumor growth, and the combination of PRXL2B knockdown and H101 produced the strongest antitumor effect. These findings indicate that PRXL2B promotes malignant phenotypes in HCC and may modulate H101 efficacy through the PI3K/AKT/PD-L1 axis. Targeting PRXL2B may therefore represent a potential strategy to enhance the therapeutic efficacy of oncolytic virus therapy in HCC.

PMID:42161529 | DOI:10.5582/bst.2026.01000

A pathogen lncRNA secreted into rice sequesters a host miRNA for virulence

✇Nature - Issue - nature.com science feeds
By: Min He · Jia Su · Xiaogang Zhou · Tuo Qi · Jiazheng Wang · Tianxin Zhang · Jinhua Chen · Mawsheng Chern · Youpin Xu · Xiang Lu · Qingqing Hou · Hongrui Liu · Wenfang Huang · Jiawei Liu · Shiying Li · Yunfei Zhu · Xue Chen · Senyu Ran · Han Li · Renju Liu · Mingliang Lei · Guosong Shu · Haicheng Liao · Junjie Yin · Xiaobo Zhu · Yongyan Tang · Li Song · Long Wang · Qing Xiong · Jiali Liu · Yu Bi · Yihua Yang · Hai Qing · Bingtian Ma · Yan Li · Jing Fan · Peng Qin · Yuping Wang · Jianming Wu · Wenming Wang · Shigui Li · Weitao Li · Jing Wang · Xuewei Chen
20 May 2026 at 08:00

Nature, Published online: 20 May 2026; doi:10.1038/s41586-026-10572-x

A fungal long non-coding RNA from Magnaporthe oryzae translocates into rice cells to sequester a host microRNA that normally represses PKR1, a negative immunity regulator, thereby facilitating infection and revealing a widespread RNA-based pathogen–host interaction mechanism.

Pixelated quantum-dot superlattice LEDs

✇Nature - Issue - nature.com science feeds
By: Chengxi Zhang · Qingsen Zeng · Hui Li · Renjun Guo · Yue Yu · Linjie Dai · Lyudmila Turyanska · Zirui Liu · Jun Dai · Yingguo Yang · Yue Zhao · Jun Lu · Lin Wang · Lingmei Kong · Tze Chien Sum · Yuchen Wu · Tae-Woo Lee · Xuyong Yang
15 April 2026 at 08:00

Nature, Published online: 15 April 2026; doi:10.1038/s41586-026-10392-z

Scalable fabrication of ordered perovskite quantum dot superlattices enables high-efficiency, ultrahigh-resolution LEDs and active-matrix displays with greatly improved brightness, stability and device lifetime.
Received — 8 April 2026 ⏭

Stabilizing Unsupervised Self-Evolution of MLLMs via Continuous Softened Retracing reSampling

✇cs.AI, q-bio.NC updates on arXiv.org
By: Yunyao Yu · Zhengxian Wu · Zhuohong Chen · Hangrui Xu · Zirui Liao · Xiangwen Deng · Zhifang Liu · Senyuan Shi · Haoqian Wang
7 April 2026 at 12:00
arXiv:2604.03647v1 Announce Type: cross Abstract: In the unsupervised self-evolution of Multimodal Large Language Models, the quality of feedback signals during post-training is pivotal for stable and effective learning. However, existing self-evolution methods predominantly rely on majority voting to select the most frequent output as the pseudo-golden answer, which may stem from the model's intrinsic biases rather than guaranteeing the objective correctness of the reasoning paths. To counteract the degradation, we propose \textbf{C}ontinuous \textbf{S}oftened \textbf{R}etracing re\textbf{S}ampling (\textbf{CSRS}) in MLLM self-evolution. Specifically, we introduce a Retracing Re-inference Mechanism (\textbf{RRM}) that the model re-inferences from anchor points to expand the exploration of long-tail reasoning paths. Simultaneously, we propose Softened Frequency Reward (\textbf{SFR}), which replaces binary rewards with continuous signals, calibrating reward based on the answers' frequency across sampled reasoning sets. Furthermore, incorporated with Visual Semantic Perturbation (\textbf{VSP}), CSRS ensures the model prioritizes mathematical logic over visual superficiality. Experimental results demonstrate that CSRS significantly enhances the reasoning performance of Qwen2.5-VL-7B on benchmarks such as MathVision. We achieve state-of-the-art (SOTA) results in unsupervised self-evolution on geometric tasks. Our code is avaible at https://github.com/yyy195/CSRS.

A Self-Evolving Defect Detection Framework for Industrial Photovoltaic Systems

✇cs.AI, q-bio.NC updates on arXiv.org
By: Haoyu He · Yu Duan · Wenzhen Liu · Hanyuan Hang · Boyu Qin · Qiantu Tuo · Xiaoke Yang · Rui Li
7 April 2026 at 12:00
arXiv:2603.14869v2 Announce Type: replace Abstract: Reliable photovoltaic (PV) power generation requires timely detection of module defects that may reduce energy yield, accelerate degradation, and increase lifecycle operation and maintenance costs during field operation. Electroluminescence (EL) imaging has therefore been widely adopted for PV module inspection. However, automated defect detection in real operational environments remains challenging due to heterogeneous module geometries, low-resolution imaging conditions, subtle defect morphology, long-tailed defect distributions, and continual data shifts introduced by evolving inspection and labeling processes. These factors significantly limit the robustness and long-term maintainability of conventional deep-learning inspection pipelines. To address these challenges, this paper proposes SEPDD, a Self-Evolving Photovoltaic Defect Detection framework designed for evolving industrial PV inspection scenarios. SEPDD integrates automated model optimization with a continual self-evolving learning mechanism, enabling the inspection system to progressively adapt to distribution shifts and newly emerging defect patterns during long-term deployment. Experiments conducted on both a public PV defect benchmark and a private industrial EL dataset demonstrate the effectiveness of the proposed framework. Both datasets exhibit severe class imbalance and significant domain shift. SEPDD achieves a leading mAP50 of 91.4% on the public dataset and 49.5% on the private dataset. It surpasses the autonomous baseline by 14.8% and human experts by 4.7% on the public dataset, and by 4.9% and 2.5%, respectively, on the private dataset.
Received — 4 April 2026 ⏭

Advances in Metabolic Reprogramming and Immune Regulatory Mechanisms in Lung Cancer

✇(Multiomics OR Omics) AND (Lung OR gastric OR Hepatocellular)
By: Xiaomeng Li · Xuejiao Li · Hongbo Wu · Rui Li
3 April 2026 at 18:00

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

Advances in Metabolic Reprogramming and Immune Regulatory Mechanisms in Lung Cancer

✇Omics In Lung
By: Xiaomeng Li · Xuejiao Li · Hongbo Wu · Rui Li
3 April 2026 at 18:00

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

CORAL: Towards Autonomous Multi-Agent Evolution for Open-Ended Discovery

✇cs.AI, q-bio.NC updates on arXiv.org
By: Ao Qu · Han Zheng · Zijian Zhou · Yihao Yan · Yihong Tang · Shao Yong Ong · Fenglu Hong · Kaichen Zhou · Chonghe Jiang · Minwei Kong · Jiacheng Zhu · Xuan Jiang · Sirui Li · Cathy Wu · Bryan Kian Hsiang Low · Jinhua Zhao · Paul Pu Liang
3 April 2026 at 12:00
arXiv:2604.01658v1 Announce Type: new Abstract: Large language model (LLM)-based evolution is a promising approach for open-ended discovery, where progress requires sustained search and knowledge accumulation. Existing methods still rely heavily on fixed heuristics and hard-coded exploration rules, which limit the autonomy of LLM agents. We present CORAL, the first framework for autonomous multi-agent evolution on open-ended problems. CORAL replaces rigid control with long-running agents that explore, reflect, and collaborate through shared persistent memory, asynchronous multi-agent execution, and heartbeat-based interventions. It also provides practical safeguards, including isolated workspaces, evaluator separation, resource management, and agent session and health management. Evaluated on diverse mathematical, algorithmic, and systems optimization tasks, CORAL sets new state-of-the-art results on 10 tasks, achieving 3-10 times higher improvement rates with far fewer evaluations than fixed evolutionary search baselines across tasks. On Anthropic's kernel engineering task, four co-evolving agents improve the best known score from 1363 to 1103 cycles. Mechanistic analyses further show how these gains arise from knowledge reuse and multi-agent exploration and communication. Together, these results suggest that greater agent autonomy and multi-agent evolution can substantially improve open-ended discovery. Code is available at https://github.com/Human-Agent-Society/CORAL.

ATBench: A Diverse and Realistic Trajectory Benchmark for Long-Horizon Agent Safety

✇cs.AI, q-bio.NC updates on arXiv.org
By: Yu Li · Haoyu Luo · Yuejin Xie · Yuqian Fu · Zhonghao Yang · Shuai Shao · Qihan Ren · Wanying Qu · Yanwei Fu · Yujiu Yang · Jing Shao · Xia Hu · Dongrui Liu
3 April 2026 at 12:00
arXiv:2604.02022v1 Announce Type: new Abstract: Evaluating the safety of LLM-based agents is increasingly important because risks in realistic deployments often emerge over multi-step interactions rather than isolated prompts or final responses. Existing trajectory-level benchmarks remain limited by insufficient interaction diversity, coarse observability of safety failures, and weak long-horizon realism. We introduce ATBench, a trajectory-level benchmark for structured, diverse, and realistic evaluation of agent safety. ATBench organizes agentic risk along three dimensions: risk source, failure mode, and real-world harm. Based on this taxonomy, we construct trajectories with heterogeneous tool pools and a long-context delayed-trigger protocol that captures realistic risk emergence across multiple stages. The benchmark contains 1,000 trajectories (503 safe and 497 unsafe), averaging 9.01 turns and 3.95k tokens, with 1,954 invoked tools drawn from pools spanning 2,084 available tools. Data quality is supported by rule-based and LLM-based filtering plus full human audit. Experiments on frontier LLMs, open-source models, and specialized guard systems show that ATBench is challenging even for strong evaluators, while enabling taxonomy-stratified analysis, cross-benchmark comparison, and diagnosis of long-horizon failure patterns.
Received — 2 April 2026 ⏭

Accelerating Diffusion Large Language Models with SlowFast Sampling: The Three Golden Principles

✇cs.AI, q-bio.NC updates on arXiv.org
By: Qingyan Wei · Yaojie Zhang · Zhiyuan Liu · Puyu Zeng · Yuxuan Wang · Biqing Qi · Dongrui Liu · Linfeng Zhang
1 April 2026 at 12:00
arXiv:2506.10848v3 Announce Type: replace-cross Abstract: Diffusion-based language models (dLLMs) have emerged as a promising alternative to traditional autoregressive LLMs by enabling parallel token generation and significantly reducing inference latency. However, existing sampling strategies for dLLMs, such as confidence-based or semi-autoregressive decoding, often suffer from static behavior, leading to suboptimal efficiency and limited flexibility. In this paper, we propose SlowFast Sampling, a novel dynamic sampling strategy that adaptively alternates between exploratory and accelerated decoding stages. Our method is guided by three golden principles: certainty principle, convergence principle, and positional principle, which govern when and where tokens can be confidently and efficiently decoded. We further integrate our strategy with dLLM-Cache to reduce redundant computation. Extensive experiments across benchmarks and models show that SlowFast Sampling achieves up to 15.63$\times$ speedup on LLaDA with minimal accuracy drop, and up to 34.22$\times$ when combined with caching. Notably, our approach outperforms strong autoregressive baselines like LLaMA3 8B in throughput, demonstrating that well-designed sampling can unlock the full potential of dLLMs for fast and high-quality generation.

Dynamic Targetable Extracellular Vesicle Surface Proteins Monitor Depth of Response to CAR T Therapy

✇MRD
By: Chen Zhao · Lei Qiu · Ning An · Yong Ju · Jacqueline Ziqian Yang · Hyoyong Kim · Ryan Y Zhang · Junseok Lee · Jingjing He · Liang-Yan Chen · Yaya Xu · Yue Ma · Emily Ren · Sophie Pan · Pranay Sashikanth · Jina Kim · Di Wang · Peiling Zhang · Jianlin Hu · Yang Gao · Yuhan Bao · Yanhua Tu · Li Wang · Zhili Wang · Zhicheng Zhang · Renjun Pei · Edwin M Posadas · Sungyong You · Wanxing Chai-Ho · Tasha L Lin · Sarah M Larson · Dinesh S Rao · Hsian-Rong Tseng · Na Sun · Chunrui Li · Yazhen Zhu
27 March 2026 at 18:00

Res Sq [Preprint]. 2026 Mar 18:rs.3.rs-8913641. doi: 10.21203/rs.3.rs-8913641/v1.

ABSTRACT

Extracellular vesicles (EVs) represent a promising liquid biopsy platform in multiple myeloma (MM). We developed an MM EV Surface Protein Assay to quantify and dynamically monitor four MM EV subpopulations defined by targetable MM surface proteins (BCMA, CD38, GPRC5D, and CD319) across 336 serial blood samples from 45 relapsed/refractory MM (RRMM) patients treated with anti-BCMA chimeric antigen receptor (CAR) T-cell therapy. All four MM EV subpopulations significantly decreased in 43 patients with initial response, while BCMA+, GPRC5D+, and CD319+ MM EVs increased in 19 patients with progression, and antigen escape was detected by BCMA+ MM EVs. MM EV subpopulations differentiated minimal residual disease (MRD) status and complemented MRD for detecting early relapse before clinical progression. Notably, CD319+ MM EVs were early predictors of progression-free and overall survival in MRD-negative patients. This assay enables noninvasive monitoring of deep response, progression, and antigen escape, and stratifies survival in MRD-negative patients with RRMM.

PMID:41890853 | PMC:PMC13015583 | DOI:10.21203/rs.3.rs-8913641/v1

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