Normal view
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cs.AI, q-bio.NC updates on arXiv.org
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Occamy-1.0: Open Pareto-frontier 35B Intelligence for Co-work
arXiv:2609.11977v1 Announce Type: new Abstract: Co-work agents execute complex workflows that combine information gathering, tool use, coding, and file manipulation across many model invocations. Because cost and latency accumulate over the full episode, their practical value depends not only on peak capability but also on how efficiently that capability is delivered. Yet many steps in everyday work emphasize state tracking, coordination, recovery, and follow-through rather than frontier-scale
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cs.AI, q-bio.NC updates on arXiv.org
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Unified Text-Image Generation with Weakness-Targeted Post-Training
arXiv:2601.04339v3 Announce Type: replace-cross Abstract: Unified multimodal generation architectures that jointly produce text and images have recently emerged as a promising direction for text-to-image (T2I) synthesis. However, many existing systems rely on explicit modality switching, generating reasoning text before switching manually to image generation. This separate, sequential inference process limits cross-modal coupling and prohibits automatic multimodal generation. This work explores
Unified Text-Image Generation with Weakness-Targeted Post-Training
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(Multiomics OR Omics) AND (Lung OR gastric OR Hepatocellular)
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A programmed cell death learning signature predicts immunotherapy response and identifies AP1S1 as a regulator of immune exclusion in breast cancer
Chin J Cancer Res. 2026 Aug 30;38(4):480-500. doi: 10.21147/j.issn.1000-9604.2026.04.08.ABSTRACTOBJECTIVE: Breast cancer remains a leading cause of global cancer mortality, characterized by profound heterogeneity. While immune checkpoint blockade (ICB) has transformed oncology, its efficacy in breast cancer is often hindered by "immune-cold" microenvironments and immune exclusion. Programmed cell death (PCD) is a critical regulator of tumor immune microenvironment (TIME). However, its role in th
A programmed cell death learning signature predicts immunotherapy response and identifies AP1S1 as a regulator of immune exclusion in breast cancer
Chin J Cancer Res. 2026 Aug 30;38(4):480-500. doi: 10.21147/j.issn.1000-9604.2026.04.08.
ABSTRACT
OBJECTIVE: Breast cancer remains a leading cause of global cancer mortality, characterized by profound heterogeneity. While immune checkpoint blockade (ICB) has transformed oncology, its efficacy in breast cancer is often hindered by "immune-cold" microenvironments and immune exclusion. Programmed cell death (PCD) is a critical regulator of tumor immune microenvironment (TIME). However, its role in the breast cancer immune microenvironment remains poorly understood.
METHODS: We integrated multi-omics data from six breast cancer cohorts (N=3,764) to develop a programmed cell death learning signature (PCDsig) using over 100 machine learning combinations. The model was benchmarked against 29 published signatures. Single-cell transcriptomic analysis decoded the immune landscape and cellular crosstalk. The role of adaptor-related protein complex 1 subunit sigma 1 (AP1S1) was validated through a clinical cohort, in vitro functional assays, and in vivo syngeneic mouse models.
RESULTS: PCDsig significantly stratified patient prognosis across all cohorts, consistently outperforming 29 existing models. High PCDsig scores correlated with immune-excluded phenotypes, reduced CD8+ T cell infiltration, and lower immunophenoscores. Single-cell analysis revealed that high-PCDsig tumors utilize vascular endothelial growth factor A (VEGFA) signaling to foster an immunosuppressive microenvironment. AP1S1 was identified as the core driver of immune exclusion. And our clinical cohort supported the immune exclusion effect of AP1S1. AP1S1 knockdown impaired tumor progression in vitro and fundamentally remodeled the tumor immune ecosystem in vivo. Combining AP1S1 inhibition with anti-programmed cell death ligand 1 (anti-PD-L1) therapy exerted profound synergistic effects, driven by massive infiltration and functional activation of cytotoxic Granzyme B (GZMB)+CD8+ T cells.
CONCLUSIONS: Our study establishes the PCDsig we developed is a potential prognostic and predictive biomarker for breast cancer. We provide the first evidence of AP1S1 as a core immunomodulatory oncogene that mediates immune exclusion. Targeting AP1S1 represents a highly promising strategy to sensitize cold breast tumors to ICB, offering a new perspective for precision immunotherapy.
PMID:42712842 | PMC:PMC13551362 | DOI:10.21147/j.issn.1000-9604.2026.04.08
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(Multiomics OR Omics) AND (Pancreatic)
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A programmed cell death learning signature predicts immunotherapy response and identifies AP1S1 as a regulator of immune exclusion in breast cancer
Chin J Cancer Res. 2026 Aug 30;38(4):480-500. doi: 10.21147/j.issn.1000-9604.2026.04.08.ABSTRACTOBJECTIVE: Breast cancer remains a leading cause of global cancer mortality, characterized by profound heterogeneity. While immune checkpoint blockade (ICB) has transformed oncology, its efficacy in breast cancer is often hindered by "immune-cold" microenvironments and immune exclusion. Programmed cell death (PCD) is a critical regulator of tumor immune microenvironment (TIME). However, its role in th
A programmed cell death learning signature predicts immunotherapy response and identifies AP1S1 as a regulator of immune exclusion in breast cancer
Chin J Cancer Res. 2026 Aug 30;38(4):480-500. doi: 10.21147/j.issn.1000-9604.2026.04.08.
ABSTRACT
OBJECTIVE: Breast cancer remains a leading cause of global cancer mortality, characterized by profound heterogeneity. While immune checkpoint blockade (ICB) has transformed oncology, its efficacy in breast cancer is often hindered by "immune-cold" microenvironments and immune exclusion. Programmed cell death (PCD) is a critical regulator of tumor immune microenvironment (TIME). However, its role in the breast cancer immune microenvironment remains poorly understood.
METHODS: We integrated multi-omics data from six breast cancer cohorts (N=3,764) to develop a programmed cell death learning signature (PCDsig) using over 100 machine learning combinations. The model was benchmarked against 29 published signatures. Single-cell transcriptomic analysis decoded the immune landscape and cellular crosstalk. The role of adaptor-related protein complex 1 subunit sigma 1 (AP1S1) was validated through a clinical cohort, in vitro functional assays, and in vivo syngeneic mouse models.
RESULTS: PCDsig significantly stratified patient prognosis across all cohorts, consistently outperforming 29 existing models. High PCDsig scores correlated with immune-excluded phenotypes, reduced CD8+ T cell infiltration, and lower immunophenoscores. Single-cell analysis revealed that high-PCDsig tumors utilize vascular endothelial growth factor A (VEGFA) signaling to foster an immunosuppressive microenvironment. AP1S1 was identified as the core driver of immune exclusion. And our clinical cohort supported the immune exclusion effect of AP1S1. AP1S1 knockdown impaired tumor progression in vitro and fundamentally remodeled the tumor immune ecosystem in vivo. Combining AP1S1 inhibition with anti-programmed cell death ligand 1 (anti-PD-L1) therapy exerted profound synergistic effects, driven by massive infiltration and functional activation of cytotoxic Granzyme B (GZMB)+CD8+ T cells.
CONCLUSIONS: Our study establishes the PCDsig we developed is a potential prognostic and predictive biomarker for breast cancer. We provide the first evidence of AP1S1 as a core immunomodulatory oncogene that mediates immune exclusion. Targeting AP1S1 represents a highly promising strategy to sensitize cold breast tumors to ICB, offering a new perspective for precision immunotherapy.
PMID:42712842 | PMC:PMC13551362 | DOI:10.21147/j.issn.1000-9604.2026.04.08
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cs.AI, q-bio.NC updates on arXiv.org
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Flow-OPD: On-Policy Distillation for Flow Matching Models
arXiv:2605.08063v5 Announce Type: replace-cross Abstract: Existing Flow Matching (FM) text-to-image models suffer from two critical bottlenecks under multi-task alignment: the reward sparsity induced by scalar-valued rewards, and the gradient interference arising from jointly optimizing heterogeneous objectives, which together give rise to a 'seesaw effect' of competing metrics and pervasive reward hacking. Inspired by the success of On-Policy Distillation (OPD) in the large language model comm
Flow-OPD: On-Policy Distillation for Flow Matching Models
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Omics in Gastric
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FDX1 as a predictive biomarker and therapeutic target for lymph node metastasis in gastric cancer
Clin Exp Med. 2026 May 10. doi: 10.1007/s10238-026-02160-0. Online ahead of print.ABSTRACTThe prognostic values of cuproptosis-related genes (CRGs) in gastric cancer with lymph node metastasis (GCLM), especially in the tumor immune microenvironment (TIME), remain unclear. We analyzed the expression, mutation, immunity, drug sensitivity, and prognostic value of CRGs in GCLM using TCGA and GEO cohorts. Consensus clustering was performed to identify CRG subtypes, with differences characterized by m
FDX1 as a predictive biomarker and therapeutic target for lymph node metastasis in gastric cancer
Clin Exp Med. 2026 May 10. doi: 10.1007/s10238-026-02160-0. Online ahead of print.
ABSTRACT
The prognostic values of cuproptosis-related genes (CRGs) in gastric cancer with lymph node metastasis (GCLM), especially in the tumor immune microenvironment (TIME), remain unclear. We analyzed the expression, mutation, immunity, drug sensitivity, and prognostic value of CRGs in GCLM using TCGA and GEO cohorts. Consensus clustering was performed to identify CRG subtypes, with differences characterized by multi-omics analysis. A CRG-based prognostic risk score and immune score were constructed for individualized assessment, and the role of CRGs was validated through in vitro and in vivo experiments. Consensus clustering revealed that CRGs were significantly enriched in biological processes related to mitosis and energy metabolism, as well as in immune-related and cancer-associated pathways. Four distinct CRG subtypes were identified, showing marked differences in expression profiles, prognosis, genetic alterations, TIME, and chemotherapeutic drug sensitivity. We developed an exploratory CRG-based prognostic risk score for preliminary individualized assessment, and the functional relevance of CRGs in GCLM was further validated through in vitro experiments. Among these, FDX1, LIAS, DLAT, MTF1, and GLS were identified as key determinants of overall survival in patients with GCLM, with FDX1 emerging as a potential independent prognostic factor. Notably, upregulation of FDX1 significantly suppressed lymph node metastasis of gastric cancer cells in a mouse popliteal lymph node metastasis model. Our data uncovers FDX1 might be a potential favorable prognostic factors in GCLM patients. These findings may improve our understanding of CRGs in GCLM and provide new in-sights for assessing prognosis and developing more effective treatment strategies.
PMID:42107026 | DOI:10.1007/s10238-026-02160-0
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Cell Death Discovery nature.com science feeds
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CX3CR1-mediated immune networks in sepsis: implications for precision therapy
Cell Death Discovery, Published online: 11 April 2026; doi:10.1038/s41420-026-03102-1CX3CR1-mediated immune networks in sepsis: implications for precision therapy
CX3CR1-mediated immune networks in sepsis: implications for precision therapy
Cell Death Discovery, Published online: 11 April 2026; doi:10.1038/s41420-026-03102-1
CX3CR1-mediated immune networks in sepsis: implications for precision therapy-
Oncogene - Issue - nature.com science feeds
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PIAS4 inhibition induces cell cycle arrest and exhibits a synergistic effect in combination with CDK4/6 inhibitor in breast cancer treatment
Oncogene, Published online: 07 April 2026; doi:10.1038/s41388-026-03753-5PIAS4 inhibition induces cell cycle arrest and exhibits a synergistic effect in combination with CDK4/6 inhibitor in breast cancer treatment
PIAS4 inhibition induces cell cycle arrest and exhibits a synergistic effect in combination with CDK4/6 inhibitor in breast cancer treatment
Oncogene, Published online: 07 April 2026; doi:10.1038/s41388-026-03753-5
PIAS4 inhibition induces cell cycle arrest and exhibits a synergistic effect in combination with CDK4/6 inhibitor in breast cancer treatment-
cs.AI, q-bio.NC updates on arXiv.org
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Learning to Learn-at-Test-Time: Language Agents with Learnable Adaptation Policies
arXiv:2604.00830v2 Announce Type: replace-cross Abstract: Test-Time Learning (TTL) enables language agents to iteratively refine their performance through repeated interactions with the environment at inference time. At the core of TTL is an adaptation policy that updates the actor policy based on experience from previous episodes, thereby improving future behavior. Existing methods rely on fixed, hand-crafted adaptation policies rather than optimizing them for downstream improvement. We argue
Learning to Learn-at-Test-Time: Language Agents with Learnable Adaptation Policies
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Journal of Medical Internet Research
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Accuracy of Radiomics-Based Machine Learning for Predicting Risk of Recurrence in Non–Small Cell Lung Cancer: Systematic Review and Meta-Analysis
Background: During the diagnosis and treatment of non–small cell lung cancer (NSCLC), detecting the risk of its recurrence in an early phase is still challenging. Recent studies have investigated the radiomics-based machine learning (ML) models for detecting the risk of recurrence in NSCLC. However, there is still insufficient systematic evidence to prove its efficiency. Objective: This study is designed to systematically evaluate the effectiveness of radiomics-based ML in predicting the risk of
Accuracy of Radiomics-Based Machine Learning for Predicting Risk of Recurrence in Non–Small Cell Lung Cancer: Systematic Review and Meta-Analysis
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cs.AI, q-bio.NC updates on arXiv.org
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Vision-DeepResearch: Incentivizing DeepResearch Capability in Multimodal Large Language Models
arXiv:2601.22060v3 Announce Type: replace-cross Abstract: Multimodal large language models (MLLMs) have achieved remarkable success across a broad range of vision tasks. However, constrained by the capacity of their internal world knowledge, prior work has proposed augmenting MLLMs by ``reasoning-then-tool-call'' for visual and textual search engines to obtain substantial gains on tasks requiring extensive factual information. However, these approaches typically define multimodal search in a na
Vision-DeepResearch: Incentivizing DeepResearch Capability in Multimodal Large Language Models
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(Multiomics OR Omics) AND (Lung OR gastric OR Hepatocellular)
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Fluid-Derived Organoids from Pleural Effusion and Ascites: Emerging Models for Drug Resistance and Personalized Oncology
J Cancer. 2026 Mar 4;17(3):614-625. doi: 10.7150/jca.127511. eCollection 2026.ABSTRACTMalignant pleural effusion (MPE) and malignant ascites (MA) are common complications in advanced-stage cancers, often signifying disease progression and resistance to treatment. Compared to tissue biopsies or surgical specimens, materials derived from effusions offer advantages such as minimal invasiveness, ease of accessibility, and the feasibility of repeated collection during therapeutic interventions. Organ
Fluid-Derived Organoids from Pleural Effusion and Ascites: Emerging Models for Drug Resistance and Personalized Oncology
J Cancer. 2026 Mar 4;17(3):614-625. doi: 10.7150/jca.127511. eCollection 2026.
ABSTRACT
Malignant pleural effusion (MPE) and malignant ascites (MA) are common complications in advanced-stage cancers, often signifying disease progression and resistance to treatment. Compared to tissue biopsies or surgical specimens, materials derived from effusions offer advantages such as minimal invasiveness, ease of accessibility, and the feasibility of repeated collection during therapeutic interventions. Organoids generated from tumor cells in effusions, termed fluid-derived organoids (FDOs), have demonstrated the ability to maintain genetic heterogeneity and accurately replicate patient-specific tumor phenotypes. These characteristics position FDOs as promising models for investigating drug resistance mechanisms and informing personalized oncology strategies. In the context of lung cancer, organoids derived from pleural effusions have been employed to study acquired resistance to epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors and immunotherapy. Similarly, in ovarian and gastrointestinal cancers, organoids derived from ascites have proven to be valuable platforms for examining chemotherapy resistance and conducting drug sensitivity testing. FDOs have shown significant potential for translational applications by effectively correlating ex vivo drug responses with clinical outcomes, thus facilitating real-time monitoring of resistance evolution. However, several challenges remain, such as achieving culture standardization, maintaining the integrity of tumor microenvironment components, and integrating with multi-omics approaches. This review provides a comprehensive overview of recent advancements in the use of pleural effusion- and ascites-derived organoids for drug resistance research, underscores their applications in personalized oncology, and explores future research directions.
PMID:41869438 | PMC:PMC13003542 | DOI:10.7150/jca.127511
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Omics In Lung
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Fluid-Derived Organoids from Pleural Effusion and Ascites: Emerging Models for Drug Resistance and Personalized Oncology
J Cancer. 2026 Mar 4;17(3):614-625. doi: 10.7150/jca.127511. eCollection 2026.ABSTRACTMalignant pleural effusion (MPE) and malignant ascites (MA) are common complications in advanced-stage cancers, often signifying disease progression and resistance to treatment. Compared to tissue biopsies or surgical specimens, materials derived from effusions offer advantages such as minimal invasiveness, ease of accessibility, and the feasibility of repeated collection during therapeutic interventions. Organ
Fluid-Derived Organoids from Pleural Effusion and Ascites: Emerging Models for Drug Resistance and Personalized Oncology
J Cancer. 2026 Mar 4;17(3):614-625. doi: 10.7150/jca.127511. eCollection 2026.
ABSTRACT
Malignant pleural effusion (MPE) and malignant ascites (MA) are common complications in advanced-stage cancers, often signifying disease progression and resistance to treatment. Compared to tissue biopsies or surgical specimens, materials derived from effusions offer advantages such as minimal invasiveness, ease of accessibility, and the feasibility of repeated collection during therapeutic interventions. Organoids generated from tumor cells in effusions, termed fluid-derived organoids (FDOs), have demonstrated the ability to maintain genetic heterogeneity and accurately replicate patient-specific tumor phenotypes. These characteristics position FDOs as promising models for investigating drug resistance mechanisms and informing personalized oncology strategies. In the context of lung cancer, organoids derived from pleural effusions have been employed to study acquired resistance to epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors and immunotherapy. Similarly, in ovarian and gastrointestinal cancers, organoids derived from ascites have proven to be valuable platforms for examining chemotherapy resistance and conducting drug sensitivity testing. FDOs have shown significant potential for translational applications by effectively correlating ex vivo drug responses with clinical outcomes, thus facilitating real-time monitoring of resistance evolution. However, several challenges remain, such as achieving culture standardization, maintaining the integrity of tumor microenvironment components, and integrating with multi-omics approaches. This review provides a comprehensive overview of recent advancements in the use of pleural effusion- and ascites-derived organoids for drug resistance research, underscores their applications in personalized oncology, and explores future research directions.
PMID:41869438 | PMC:PMC13003542 | DOI:10.7150/jca.127511
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Oncogene - Issue - nature.com science feeds
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Aryl hydrocarbon receptor is critical for both AR-dependent and AR-indifferent enzalutamide resistance in castration-resistant prostate cancer
Oncogene, Published online: 23 March 2026; doi:10.1038/s41388-026-03723-xAryl hydrocarbon receptor is critical for both AR-dependent and AR-indifferent enzalutamide resistance in castration-resistant prostate cancer
Aryl hydrocarbon receptor is critical for both AR-dependent and AR-indifferent enzalutamide resistance in castration-resistant prostate cancer
Oncogene, Published online: 23 March 2026; doi:10.1038/s41388-026-03723-x
Aryl hydrocarbon receptor is critical for both AR-dependent and AR-indifferent enzalutamide resistance in castration-resistant prostate cancer-
Omics In Lung
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Extracellular Vesicles in Osteosarcoma: Mechanisms, Diagnostics and Therapeutic Applications
Drug Des Devel Ther. 2026 Jan 6;20:565059. doi: 10.2147/DDDT.S565059. eCollection 2026.ABSTRACTOsteosarcoma is a primary bone malignancy of adolescents and young adults with marked heterogeneity and a high metastatic propensity. Five-year survival exceeds 70% in localized disease but falls to about 20% with pulmonary metastasis or chemoresistance, and overall outcomes have plateaued for decades. Extracellular vesicles (EVs) have emerged as critical mediators of osteosarcoma progression and metas
Extracellular Vesicles in Osteosarcoma: Mechanisms, Diagnostics and Therapeutic Applications
Drug Des Devel Ther. 2026 Jan 6;20:565059. doi: 10.2147/DDDT.S565059. eCollection 2026.
ABSTRACT
Osteosarcoma is a primary bone malignancy of adolescents and young adults with marked heterogeneity and a high metastatic propensity. Five-year survival exceeds 70% in localized disease but falls to about 20% with pulmonary metastasis or chemoresistance, and overall outcomes have plateaued for decades. Extracellular vesicles (EVs) have emerged as critical mediators of osteosarcoma progression and metastasis. EVs remodel the tumor microenvironment (TME) by promoting immune evasion, extracellular matrix reprogramming, and angiogenesis, while also facilitating invasion, epithelial-mesenchymal transition (EMT)-like plasticity, and formation of lung pre-metastatic niches through organotropic integrins and glycoproteins. Their cargo, including proteins, lipids, and nucleic acids, drives intercellular communication that sustains proliferation, migration, and therapy resistance under metabolic or hypoxic stress. Clinically, the stability of EVs in body fluids and their tumor-specific molecular signatures highlight their promise as liquid-biopsy biomarkers for early diagnosis, prognosis, and treatment monitoring. Therapeutically, EVs are being engineered as delivery vehicles for drugs or RNA therapeutics, and interventions targeting their biogenesis, cargo sorting, or uptake are under exploration. Future research should integrate single-EV multi-omics, longitudinal cohort validation, and causal perturbation models to delineate functional mechanisms. Rational strategies that modulate EV dynamics and incorporate standardized analytic pipelines may transform EVs into actionable biomarkers and therapeutic targets, offering new avenues to overcome resistance and improve clinical outcomes in osteosarcoma.
PMID:41858917 | PMC:PMC12998350 | DOI:10.2147/DDDT.S565059
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Oncogene - Issue - nature.com science feeds
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LINC-AC092535.5 regulates MICAL2 mRNA level to inhibit p53-mediated ferroptosis in nasopharyngeal carcinoma
Oncogene, Published online: 14 March 2026; doi:10.1038/s41388-026-03714-yLINC-AC092535.5 regulates MICAL2 mRNA level to inhibit p53-mediated ferroptosis in nasopharyngeal carcinoma
LINC-AC092535.5 regulates MICAL2 mRNA level to inhibit p53-mediated ferroptosis in nasopharyngeal carcinoma
Oncogene, Published online: 14 March 2026; doi:10.1038/s41388-026-03714-y
LINC-AC092535.5 regulates MICAL2 mRNA level to inhibit p53-mediated ferroptosis in nasopharyngeal carcinoma-
Nature - Issue - nature.com science feeds
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Author Correction: Gut stem cell necroptosis by genome instability triggers bowel inflammation
Nature, Published online: 11 March 2026; doi:10.1038/s41586-026-10302-3Author Correction: Gut stem cell necroptosis by genome instability triggers bowel inflammation
Author Correction: Gut stem cell necroptosis by genome instability triggers bowel inflammation
Nature, Published online: 11 March 2026; doi:10.1038/s41586-026-10302-3
Author Correction: Gut stem cell necroptosis by genome instability triggers bowel inflammation-
cs.AI, q-bio.NC updates on arXiv.org
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A Novel Multi-Agent Architecture to Reduce Hallucinations of Large Language Models in Multi-Step Structural Modeling
arXiv:2603.07728v1 Announce Type: new Abstract: Large language models (LLMs) such as GPT and Gemini have demonstrated remarkable capabilities in contextual understanding and reasoning. The strong performance of LLMs has sparked growing interest in leveraging them to automate tasks traditionally dependent on human expertise. Recently, LLMs have been integrated into intelligent agents capable of operating structural analysis software (e.g., OpenSees) to construct structural models and perform ana
A Novel Multi-Agent Architecture to Reduce Hallucinations of Large Language Models in Multi-Step Structural Modeling
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cs.AI, q-bio.NC updates on arXiv.org
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xLLM Technical Report
arXiv:2510.14686v2 Announce Type: replace-cross Abstract: We introduce xLLM, an intelligent and efficient Large Language Model (LLM) inference framework designed for high-performance, large-scale enterprise-grade serving, with deep optimizations for diverse AI accelerators. To address these challenges, xLLM builds a novel decoupled service-engine architecture. At the service layer, xLLM-Service features an intelligent scheduling module that efficiently processes multimodal requests and co-locat
xLLM Technical Report
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cs.AI, q-bio.NC updates on arXiv.org
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WebDevJudge: Evaluating (M)LLMs as Critiques for Web Development Quality
arXiv:2510.18560v3 Announce Type: replace-cross Abstract: The paradigm of LLM-as-a-judge is emerging as a scalable and efficient alternative to human evaluation, demonstrating strong performance on well-defined tasks. However, its reliability in open-ended tasks with dynamic environments and complex interactions remains unexplored. To bridge the gap, we introduce WebDevJudge, a systematic benchmark for assessing LLM-as-a-judge performance in web development, with support for both non-interactiv