Normal view
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cs.AI, q-bio.NC updates on arXiv.org
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HoloFair: Unified T2I Fairness Evaluation and Fair-GRPO Debiasing
arXiv:2605.24687v1 Announce Type: cross Abstract: Text-to-Image (T2I) models have made significant strides in visual realism and semantic consistency, yet they often perpetuate and amplify societal biases. Existing evaluation methods typically address only single-dimensional biases, lacking perspectives to uncover model biases at social-related deeper semantic levels. We introduce HoloFair, a comprehensive benchmark framework for multidimensional demographic bias analysis. Built upon our large-
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Omics in Hepatocellular
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UBTF-HSP90A-MIF stress circuit drives lenvatinib resistance and immune exclusion in hepatocellular carcinoma
J Adv Res. 2026 Apr 5:S2090-1232(26)00280-8. doi: 10.1016/j.jare.2026.04.002. Online ahead of print.ABSTRACTINTRODUCTION: The clinical benefit of combining lenvatinib with PD-1 blockade in HCC is frequently constrained by adaptive resistance and the development of an immune-cold tumor microenvironment.OBJECTIVES: This study aimed to elucidate the molecular mechanisms underlying adaptive resistance and immune exclusion during lenvatinib-PD-1 therapy in HCC, with a particular focus on a UBTF/HSP90
UBTF-HSP90A-MIF stress circuit drives lenvatinib resistance and immune exclusion in hepatocellular carcinoma
J Adv Res. 2026 Apr 5:S2090-1232(26)00280-8. doi: 10.1016/j.jare.2026.04.002. Online ahead of print.
ABSTRACT
INTRODUCTION: The clinical benefit of combining lenvatinib with PD-1 blockade in HCC is frequently constrained by adaptive resistance and the development of an immune-cold tumor microenvironment.
OBJECTIVES: This study aimed to elucidate the molecular mechanisms underlying adaptive resistance and immune exclusion during lenvatinib-PD-1 therapy in HCC, with a particular focus on a UBTF/HSP90A/MIF regulatory circuit. We examined whether genetic or pharmacologic targeting of macrophage migration inhibitory factor (MIF) could restore lenvatinib sensitivity, remodel the tumor immune microenvironment, and serve as a predictive biomarker in clinical cohorts.
METHODS: Paired lenvatinib-sensitive and -resistant HCC models were interrogated using integrated multi-omic and functional approaches, including RNA sequencing, promoter pull-down assays, ChIP, luciferase reporter assays, PLA, and flow cytometry. Key findings were validated in patient-derived organoids and xenografts, as well as in an immunocompetent hydrodynamic HCC mouse model. Clinical relevance was evaluated in independent cohorts treated with lenvatinib plus anti-PD-1 therapy.
RESULTS: UBTF directly bound to and transcriptionally activated the HSP90A promoter, resulting in increased HSP90A expression and stabilization of MIF. MIF signaling through CD74 co-activated the PI3K-AKT and MAPK pathways, sustaining tumor cell proliferation under lenvatinib pressure. Single-cell RNA sequencing and multiplex immunohistochemistry revealed macrophage enrichment and CD8+ T-cell exclusion in resistant tumors. Genetic ablation of Mif (Alb-Cre; Mifflox/flox) or pharmacologic inhibition with 4-IPP (4-Iodo-6-phenylpyrimidine) restored lenvatinib sensitivity, reprogrammed the tumor immune microenvironment, and, when combined with PD-1 blockade, achieved superior tumor control and prolonged survival. In clinical datasets, low pretreatment MIF expression was associated with improved responses to lenvatinib plus PD-1 therapy.
CONCLUSIONS: These findings define a UBTF/HSP90A/MIF axis linking proteostasis and cytokine signaling to immune-metabolic dysfunction and lenvatinib resistance in HCC. MIF emerges as both a mechanistic driver and a predictive biomarker, supporting prospective evaluation of therapeutic strategies combining lenvatinib-PD-1 with MIF- or HSP90A-targeted interventions to personalize TKI-ICI therapy.
PMID:41946392 | DOI:10.1016/j.jare.2026.04.002
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cs.AI, q-bio.NC updates on arXiv.org
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CA-HFP: Curvature-Aware Heterogeneous Federated Pruning with Model Reconstruction
arXiv:2603.12591v1 Announce Type: cross Abstract: Federated learning on heterogeneous edge devices requires personalized compression while preserving aggregation compatibility and stable convergence. We present Curvature-Aware Heterogeneous Federated Pruning (CA-HFP), a practical framework that enables each client perform structured, device-specific pruning guided by a curvature-informed significance score, and subsequently maps its compact submodel back into a common global parameter space via
CA-HFP: Curvature-Aware Heterogeneous Federated Pruning with Model Reconstruction
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cs.AI, q-bio.NC updates on arXiv.org
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From Thinker to Society: Security in Hierarchical Autonomy Evolution of AI Agents
arXiv:2603.07496v1 Announce Type: cross Abstract: Artificial Intelligence (AI) agents have evolved from passive predictive tools into active entities capable of autonomous decision-making and environmental interaction, driven by the reasoning capabilities of Large Language Models (LLMs). However, this evolution has introduced critical security vulnerabilities that existing frameworks fail to address. The Hierarchical Autonomy Evolution (HAE) framework organizes agent security into three tiers:
From Thinker to Society: Security in Hierarchical Autonomy Evolution of AI Agents
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cs.AI, q-bio.NC updates on arXiv.org
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Preventing Rank Collapse in Federated Low-Rank Adaptation with Client Heterogeneity
arXiv:2602.13486v1 Announce Type: cross Abstract: Federated low-rank adaptation (FedLoRA) has facilitated communication-efficient and privacy-preserving fine-tuning of foundation models for downstream tasks. In practical federated learning scenarios, client heterogeneity in system resources and data distributions motivates heterogeneous LoRA ranks across clients. We identify a previously overlooked phenomenon in heterogeneous FedLoRA, termed rank collapse, where the energy of the global update