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cs.AI, q-bio.NC updates on arXiv.org
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RESCUE-BENCH: Towards Relation-Aware Multi-Party Emotional Support Conversation Systems
arXiv:2609.09657v1 Announce Type: new Abstract: Existing emotional support conversation systems mainly focus on one-on-one seeker-supporter interactions and individual emotional states, leaving interpersonal relations in multi-party scenarios underexplored. In this work, we introduce relation-aware emotional support conversation, a new task that evaluates whether LLMs can capture and utilize the evolving dynamics of relationships to offer more effective emotional support. We construct RESCUE (R
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(Multiomics OR Omics) AND (Lung OR gastric OR Hepatocellular)
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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
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Omics In Lung
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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
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cs.AI, q-bio.NC updates on arXiv.org
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UnfoldLDM: Deep Unfolding-based Blind Image Restoration with Latent Diffusion Priors
arXiv:2511.18152v2 Announce Type: replace-cross Abstract: Deep unfolding networks (DUNs) combine the interpretability of model-based methods with the learning ability of deep networks, yet remain limited for blind image restoration (BIR). Existing DUNs suffer from: (1) \textbf{Degradation-specific dependency}, as their optimization frameworks are tied to a known degradation model, making them unsuitable for BIR tasks; and (2) \textbf{Over-smoothing bias}, resulting from the direct feeding of gr
UnfoldLDM: Deep Unfolding-based Blind Image Restoration with Latent Diffusion Priors
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cs.AI, q-bio.NC updates on arXiv.org
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Delegation and Verification Under AI
arXiv:2603.02961v1 Announce Type: cross Abstract: As AI systems enter institutional workflows, workers must decide whether to delegate task execution to AI and how much effort to invest in verifying AI outputs, while institutions evaluate workers using outcome-based standards that may misalign with workers' private costs. We model delegation and verification as the solution to a rational worker's optimization problem, and define worker quality by evaluating an institution-centered utility (dist