Normal view
-
cs.AI, q-bio.NC updates on arXiv.org
-
Toward Robust Personalized Alignment for LLMs: Mitigating Persona Drift in Multi-Turn Dialogue
arXiv:2609.12373v1 Announce Type: new Abstract: Persona drift remains a central challenge for personalized language models, as user profiles evolve over long interactions rather than remain permanently fixed. Models must therefore revise persistent persona states when preferences genuinely change, while avoiding updates driven by transient, ambiguous, or unresolved observations. We propose CORE, which separates turn-local evidence from persistent persona-state revision and selectively updates g
-
cs.AI, q-bio.NC updates on arXiv.org
-
ShadowPEFT: Shadow Network for Parameter-Efficient Fine-Tuning
arXiv:2604.19254v2 Announce Type: replace-cross Abstract: Popular low-rank parameter-efficient fine-tuning (PEFT) methods represent adaptation as separate updates to selected backbone weights, without maintaining an explicit task-specific state that is updated and reused across depth. These updates also require the backbone at inference and therefore cannot operate as standalone predictors. We propose ShadowPEFT, which consolidates trainable adaptation into a modular shadow component centered o
ShadowPEFT: Shadow Network for Parameter-Efficient Fine-Tuning
-
cs.AI, q-bio.NC updates on arXiv.org
-
Right Family, Wrong Skill: Evaluating Risk Exposure in Agent Skill Retrieval
arXiv:2606.10388v3 Announce Type: replace-cross Abstract: Agent skill libraries are becoming routable software assets: a retrieved skill can contribute instructions, scripts, resource bindings, and execution assumptions to an agent. This makes retrieval failures more specific than broad irrelevance. A system can find the right capability family yet expose the wrong same-capability representative. We study this failure as same-capability risk-exposure retrieval. Each benchmark unit pairs a helpf
Right Family, Wrong Skill: Evaluating Risk Exposure in Agent Skill Retrieval
-
cs.AI, q-bio.NC updates on arXiv.org
-
JarvisGUI: Towards Cross-Device GUI Agents with Dynamic Task Composition
arXiv:2609.10451v1 Announce Type: new Abstract: Real-world GUI usage frequently involves workflows that span multiple devices and platforms, requiring the transfer of intermediate results, maintenance of shared state, and coordination across heterogeneous environments. However, existing GUI benchmarks overwhelmingly evaluate agents on single-device, statically defined tasks, thus leaving such cross-device capabilities largely unexamined, resulting in an overly optimistic assessment of agents' r
JarvisGUI: Towards Cross-Device GUI Agents with Dynamic Task Composition
-
cs.AI, q-bio.NC updates on arXiv.org
-
MOSAIC: A Universal Agent-Level Interface for Cross-Paradigm Agent Mixing and Human-AI Collaboration
arXiv:2603.01260v2 Announce Type: replace-cross Abstract: Existing infrastructure cannot deploy agents from different decision-making paradigms within the same environment, making fair cross-paradigm comparison under identical conditions impossible. We present MOSAIC, an open-source platform that enables heterogeneous agents (RL policies, LLMs, VLMs, and human operators) to act within shared reinforcement learning environments in ad-hoc team settings with reproducible results. MOSAIC introduces
MOSAIC: A Universal Agent-Level Interface for Cross-Paradigm Agent Mixing and Human-AI Collaboration
-
Pulmonary nodule
-
Multiomic characterization of malignant pulmonary nodules and development of a methylation-based diagnostic Model
J Transl Med. 2026 Jun 8;24(1):776. doi: 10.1186/s12967-026-08382-w.ABSTRACTBACKGROUND: The molecular distinction between benign and malignant pulmonary nodules remains a significant diagnostic challenge. While genomic drivers are well studied, multiomic integration of the epigenetic-transcriptional landscape and its translation into noninvasive tools are lacking.METHODS: We performed a multiomic characterization (genomic, epigenomic, and transcriptomic) of 158 pulmonary nodules. Unsupervised fa
Multiomic characterization of malignant pulmonary nodules and development of a methylation-based diagnostic Model
J Transl Med. 2026 Jun 8;24(1):776. doi: 10.1186/s12967-026-08382-w.
ABSTRACT
BACKGROUND: The molecular distinction between benign and malignant pulmonary nodules remains a significant diagnostic challenge. While genomic drivers are well studied, multiomic integration of the epigenetic-transcriptional landscape and its translation into noninvasive tools are lacking.
METHODS: We performed a multiomic characterization (genomic, epigenomic, and transcriptomic) of 158 pulmonary nodules. Unsupervised factor analysis integrated these layers to identify core regulatory axes. A 9-gene cell-free DNA (cfDNA) methylation classifier was developed and validated in blood and tissue cohorts.
RESULTS: Genomic profiling revealed EGFR mutations (exclusive to malignant nodules) and MYC amplification as fundamental initiators of malignancy. Multiomic factor analysis (Factor 1) revealed profound genetic‒epigenetic synergy, in which these alterations dictate a permissive methylome, leading to aberrant epigenetic programming of chromatin accessibility, as well as epigenetic-transcriptional effects: hypomethylation at the promoters of cell cycle genes that augments their expression, and hypermethylation at immune related pathways gene loci that silences their transcription. This effect orchestrates formation of proproliferative (E2F target/G2M checkpoint) and "immune-cold" malignant phenotype, characterized by elevated Treg/CD8+ ratios and fibroblast recruitment. Notably, we observed a gradual accumulation of methylation aberrations along the premalignant-to-invasive continuum (adenocarcinoma in situ [AIS]→minimally invasive adenocarcinoma [MIA]→adenocarcinoma [ADC]), identifying progressive epigenetic dysregulation as a hallmark of tumor aggressiveness. Global methylome remodeling drives ADC progression through hypermethylation-mediated silencing of tumor suppressors (RASA3 and PPARG) and hypomethylation-activated oncogenic axes, specifically the GDF15 axis, which independently predict poor survival in patients with lung ADC in the TCGA cohort. We translated these tissue-derived insights into a 9-gene cfDNA methylation classifier, which achieved exceptional diagnostic accuracy across independent cohorts (training AUC = 1.00; test AUC = 0.93; tissue AUC = 0.96). Rooted in the biological "ground truth" of tissue dysregulation, this classifier functions specifically as a functional readout of the core cell cycle and proliferative pathways, offering a robust, noninvasive tool for the biology-informed risk assessment of pulmonary nodules.
CONCLUSIONS: This study delineates an epigenetic-transcriptional regulatory network that drives nodule malignancy. Our findings provide a robust theoretical foundation and a high-performance liquid biopsy tool for the precise, noninvasive diagnosis of pulmonary nodules.
PMID:42260586 | PMC:PMC13274191 | DOI:10.1186/s12967-026-08382-w
-
(Multiomics OR Omics) AND (Lung OR gastric OR Hepatocellular)
-
A Non-Canonical Role of SMAD4 in Regulating 3D Genome Architecture to Inhibit Lung Squamous Cell Carcinoma Development
Adv Sci (Weinh). 2026 May 26:e75839. doi: 10.1002/advs.75839. Online ahead of print.ABSTRACTLung 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 datas
A Non-Canonical Role of SMAD4 in Regulating 3D Genome Architecture to Inhibit Lung Squamous Cell Carcinoma Development
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
-
Omics In Lung
-
A Non-Canonical Role of SMAD4 in Regulating 3D Genome Architecture to Inhibit Lung Squamous Cell Carcinoma Development
Adv Sci (Weinh). 2026 May 26:e75839. doi: 10.1002/advs.75839. Online ahead of print.ABSTRACTLung 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 datas
A Non-Canonical Role of SMAD4 in Regulating 3D Genome Architecture to Inhibit Lung Squamous Cell Carcinoma Development
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
-
cs.AI, q-bio.NC updates on arXiv.org
-
Parameter Efficient Multi-Class Intelligent Scheduling for Multimodal Online Distributed Industrial Anomaly Detection
arXiv:2605.23984v1 Announce Type: cross Abstract: Industrial anomaly detection has attracted significant attention as a fundamental challenge in industrial systems. The rapid advancement of heterogeneous industrial sensors has driven industrial anomaly detection from unimodal to multimodal paradigms. However, existing methods are primarily designed for centralized and offline settings, overlooking the distributed and continuously generated data characteristic of real-world industrial environmen
Parameter Efficient Multi-Class Intelligent Scheduling for Multimodal Online Distributed Industrial Anomaly Detection
-
cs.AI, q-bio.NC updates on arXiv.org
-
A World Model of Radiologist Reading for Medical Image Representation Learning
arXiv:2605.23992v1 Announce Type: cross Abstract: Radiologist eye-tracking data provide a rich record of how experts search, compare, and accumulate evidence during image reading; yet, existing methods exploit this signal only partially, either as a static spatial prior or as an auxiliary prediction target decoupled from diagnosis. We propose GazeWorld, a medical imaging world model that treats the image as the world and the radiologist's fixation sequence as a trajectory through it. GazeWorld
A World Model of Radiologist Reading for Medical Image Representation Learning
-
cs.AI, q-bio.NC updates on arXiv.org
-
Correcting Visual Blur Induced by Attention Distraction to Reduce Hallucinations: Algorithm and Theory
arXiv:2605.24602v1 Announce Type: cross Abstract: Multimodal large language models (MLLMs) frequently suffer from object hallucinations, yet the visual perceptual mechanism underlying this failure remains poorly understood. In this work, we reveal that hallucinations are strongly associated with a human-like attention distraction phenomenon, where humans under divided focus experience degraded visual clarity and produce inaccurate descriptions, while in models the same mechanism manifests as sp
Correcting Visual Blur Induced by Attention Distraction to Reduce Hallucinations: Algorithm and Theory
-
cs.AI, q-bio.NC updates on arXiv.org
-
Factorize to Generalize: Retrieval-Guided Invariant-Dynamic Decomposition for Time Series Forecasting
arXiv:2605.24911v1 Announce Type: cross Abstract: Time series foundation models (TSFMs) have recently achieved strong zero-shot forecasting performance through large-scale pretraining and retrieval-augmented prediction. However, our empirical analysis reveals a non-trivial limitation of retrieval-based forecasting: retrieval tends to induce more oscillatory predictions, improving performance on highly fluctuating series while degrading accuracy on smoother, trend-dominated ones. This suggests t
Factorize to Generalize: Retrieval-Guided Invariant-Dynamic Decomposition for Time Series Forecasting
-
cs.AI, q-bio.NC updates on arXiv.org
-
MinerU-Popo: Universal Post-Processing Model for Structured Document Parsing
arXiv:2605.24973v1 Announce Type: cross Abstract: VLM-based OCR models have become the de facto choice for document parsing, as they can accurately extract page-level elements (e.g., paragraphs within individual pages) together with their bounding boxes and textual content. However, downstream applications such as RAG require coherent document-level information, whereas these models often break cross-page continuity and fail to recover disrupted structures, such as paragraphs and tables truncat
MinerU-Popo: Universal Post-Processing Model for Structured Document Parsing
-
cs.AI, q-bio.NC updates on arXiv.org
-
CollectionLoRA: Collecting 50 Effects in 1 LoRA via Multi-Teacher On-Policy Distillation
arXiv:2605.25378v1 Announce Type: cross Abstract: Customized image editing aims to equip pre-trained diffusion models with specific visual effects using limited paired data, typically via Low-Rank Adaptation (LoRA). As the number of desired effects grows, storing and dynamically loading numerous these effect LoRAs significantly increases deployment overhead. Furthermore, current pipelines typically cascade these effect LoRAs with acceleration modules for fast generation, which triggers severe p
CollectionLoRA: Collecting 50 Effects in 1 LoRA via Multi-Teacher On-Policy Distillation
-
cs.AI, q-bio.NC updates on arXiv.org
-
Channel-wise Vector Quantization
arXiv:2605.26089v1 Announce Type: cross Abstract: We present Channel-wise Vector Quantization (CVQ), a novel image tokenization paradigm that replaces patch-wise tokens with channel-wise tokens. Unlike conventional vector quantization, which assigns a discrete token to each patch feature vector, CVQ quantizes each channel of the feature map. This formulation represents an image as discrete levels of visual details, rather than as a grid of spatial patches. Based on CVQ, we introduce a new visua
Channel-wise Vector Quantization
-
cs.AI, q-bio.NC updates on arXiv.org
-
From Prompt Optimization to Multi-Dimensional Credibility Evaluation: Enhancing Trustworthiness of Chinese LLM-Generated Liver MRI Reports -- with Preliminary Extension to Lung Cancer
arXiv:2510.23008v3 Announce Type: replace Abstract: Large language models (LLMs) have demonstrated promising performance in generating diagnostic conclusions from imaging findings, thereby supporting radiology reporting, trainee education, and quality control. However, systematic guidance on how to optimize prompt design across different clinical contexts remains underexplored. Moreover, a comprehensive and standardized framework for assessing the trustworthiness of LLM-generated radiology repo
From Prompt Optimization to Multi-Dimensional Credibility Evaluation: Enhancing Trustworthiness of Chinese LLM-Generated Liver MRI Reports -- with Preliminary Extension to Lung Cancer
-
cs.AI, q-bio.NC updates on arXiv.org
-
TimeGuard: Channel-wise Pool Training for Backdoor Defense in Time Series Forecasting
arXiv:2605.22365v2 Announce Type: replace-cross Abstract: Time Series Forecasting (TSF) is highly vulnerable to backdoor attacks, yet effective defenses remain underexplored due to challenges arising from data entanglement and shifts in task formulation. To fill this gap, we conduct a systematic evaluation of thirteen representative backdoor defenses across the TSF life cycle and analyze their failure modes. Our results reveal two fundamental issues: (1) data entanglement induces channel-level
TimeGuard: Channel-wise Pool Training for Backdoor Defense in Time Series Forecasting
-
Nature Biotechnology - Issue - nature.com science feeds
-
A framework for building a synthetic cell from the SynCell Asia Initiative
Nature Biotechnology, Published online: 26 May 2026; doi:10.1038/s41587-026-03153-wBuilding a living cell from scratch requires overcoming a bottleneck that has remained unresolved despite decades of progress: orchestrating the spatiotemporal integration of core functional modules. To tackle this barrier, the SynCell Asia Initiative outlines a strategy for developing core functional modules followed by their systems-level integration through the establishment of a centralized, artificial intelli
A framework for building a synthetic cell from the SynCell Asia Initiative
Nature Biotechnology, Published online: 26 May 2026; doi:10.1038/s41587-026-03153-w
Building a living cell from scratch requires overcoming a bottleneck that has remained unresolved despite decades of progress: orchestrating the spatiotemporal integration of core functional modules. To tackle this barrier, the SynCell Asia Initiative outlines a strategy for developing core functional modules followed by their systems-level integration through the establishment of a centralized, artificial intelligence (AI)-driven biofoundry.-
(Multiomics OR Omics) AND (Lung OR gastric OR Hepatocellular)
-
Multi-omics biomarkers for predicting resistance, hyperprogression, and immune-related toxicity during PD-1/PD-L1 therapy in lung cancer: a literature review
Front Immunol. 2026 May 8;17:1780459. doi: 10.3389/fimmu.2026.1780459. eCollection 2026.ABSTRACTImmune checkpoint inhibitors targeting programmed cell death protein 1 (PD-1) and its ligand programmed death-ligand 1 (PD-L1) have transformed the management of advanced lung cancer, yet most patients experience primary resistance, hyperprogressive disease (HPD), or clinically significant immune-related adverse events (irAEs). Multi-omics technologies now enable integrated interrogation of tumor, mic
Multi-omics biomarkers for predicting resistance, hyperprogression, and immune-related toxicity during PD-1/PD-L1 therapy in lung cancer: a literature review
Front Immunol. 2026 May 8;17:1780459. doi: 10.3389/fimmu.2026.1780459. eCollection 2026.
ABSTRACT
Immune checkpoint inhibitors targeting programmed cell death protein 1 (PD-1) and its ligand programmed death-ligand 1 (PD-L1) have transformed the management of advanced lung cancer, yet most patients experience primary resistance, hyperprogressive disease (HPD), or clinically significant immune-related adverse events (irAEs). Multi-omics technologies now enable integrated interrogation of tumor, microenvironmental, host, and clinical determinants of these divergent outcomes. In this review, we first discuss the biological and clinical foundations of PD-1/PD-L1 blockade in non-small cell and small cell lung cancer, and summarize the spectrum of resistance, HPD, and irAEs observed in trials and real-world practice. We then describe multi-omics study frameworks that connect genomics, transcriptomics, epigenomics, proteomics, metabolomics, radiomics, and microbiome profiling with these outcome phenotypes. Building on this foundation, we synthesize evidence for composite biomarkers of primary and acquired resistance, delineate emerging multi-omics signatures of HPD, and examine host- and tumor-derived multi-omics correlates of organ-specific and systemic irAEs. We further propose an efficacy-risk quadrant framework to guide clinical decision-making when favorable efficacy predictors coexist with elevated risk of severe adverse outcomes, and outline a three-step approach for high-efficacy/high-risk patients: joint probability reporting, multi-omics guided mitigation, and dynamic reassessment. Finally, we evaluate translational strategies that integrate multi-omics scores into baseline risk stratification, dynamic monitoring with attention to technical challenges such as distinguishing true progression from ctDNA pseudoprogression, and biomarker-driven trial design, while assessing the evidence level and translational readiness of candidate assays from retrospective discovery to clinical implementation. A clinical case illustrates how multi-omics can link baseline risk stratification, regimen selection, and longitudinal monitoring into a coherent action plan, while acknowledging that artificial intelligence-driven models remain investigational and real-world application still relies on clinician judgment. Collectively, this review defines how integrated multi-omics biomarkers can be leveraged to predict resistance, HPD, and immune-related toxicity, and to refine patient selection and management during PD-1/PD-L1 therapy in lung cancer.
PMID:42183274 | PMC:PMC13194140 | DOI:10.3389/fimmu.2026.1780459
-
Omics In Lung
-
Multi-omics biomarkers for predicting resistance, hyperprogression, and immune-related toxicity during PD-1/PD-L1 therapy in lung cancer: a literature review
Front Immunol. 2026 May 8;17:1780459. doi: 10.3389/fimmu.2026.1780459. eCollection 2026.ABSTRACTImmune checkpoint inhibitors targeting programmed cell death protein 1 (PD-1) and its ligand programmed death-ligand 1 (PD-L1) have transformed the management of advanced lung cancer, yet most patients experience primary resistance, hyperprogressive disease (HPD), or clinically significant immune-related adverse events (irAEs). Multi-omics technologies now enable integrated interrogation of tumor, mic
Multi-omics biomarkers for predicting resistance, hyperprogression, and immune-related toxicity during PD-1/PD-L1 therapy in lung cancer: a literature review
Front Immunol. 2026 May 8;17:1780459. doi: 10.3389/fimmu.2026.1780459. eCollection 2026.
ABSTRACT
Immune checkpoint inhibitors targeting programmed cell death protein 1 (PD-1) and its ligand programmed death-ligand 1 (PD-L1) have transformed the management of advanced lung cancer, yet most patients experience primary resistance, hyperprogressive disease (HPD), or clinically significant immune-related adverse events (irAEs). Multi-omics technologies now enable integrated interrogation of tumor, microenvironmental, host, and clinical determinants of these divergent outcomes. In this review, we first discuss the biological and clinical foundations of PD-1/PD-L1 blockade in non-small cell and small cell lung cancer, and summarize the spectrum of resistance, HPD, and irAEs observed in trials and real-world practice. We then describe multi-omics study frameworks that connect genomics, transcriptomics, epigenomics, proteomics, metabolomics, radiomics, and microbiome profiling with these outcome phenotypes. Building on this foundation, we synthesize evidence for composite biomarkers of primary and acquired resistance, delineate emerging multi-omics signatures of HPD, and examine host- and tumor-derived multi-omics correlates of organ-specific and systemic irAEs. We further propose an efficacy-risk quadrant framework to guide clinical decision-making when favorable efficacy predictors coexist with elevated risk of severe adverse outcomes, and outline a three-step approach for high-efficacy/high-risk patients: joint probability reporting, multi-omics guided mitigation, and dynamic reassessment. Finally, we evaluate translational strategies that integrate multi-omics scores into baseline risk stratification, dynamic monitoring with attention to technical challenges such as distinguishing true progression from ctDNA pseudoprogression, and biomarker-driven trial design, while assessing the evidence level and translational readiness of candidate assays from retrospective discovery to clinical implementation. A clinical case illustrates how multi-omics can link baseline risk stratification, regimen selection, and longitudinal monitoring into a coherent action plan, while acknowledging that artificial intelligence-driven models remain investigational and real-world application still relies on clinician judgment. Collectively, this review defines how integrated multi-omics biomarkers can be leveraged to predict resistance, HPD, and immune-related toxicity, and to refine patient selection and management during PD-1/PD-L1 therapy in lung cancer.
PMID:42183274 | PMC:PMC13194140 | DOI:10.3389/fimmu.2026.1780459