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PhysCodeBench: Benchmarking Physics-Aware Symbolic Simulation of 3D Scenes via Self-Corrective Multi-Agent Refinement
Propionyl-CoA catabolism is a metabolic gatekeeper for fatty acid oxidation in pancreatic cancer
Oncogene, Published online: 11 September 2026; doi:10.1038/s41388-026-03979-3
Propionyl-CoA catabolism is a metabolic gatekeeper for fatty acid oxidation in pancreatic cancerThe Effectiveness of Digital Intervention on Psychological Resilience in Postoperative Breast Cancer Patients During Chemotherapy Intervals: Quasi-Experimental Study
Transduction Efficiency in Clinical CAR T-Cell Products: A Retrospective Study at a Single Center
The DreAM-plus integrative RNA switch enhances transient AAV expression and reduces side effects of gene editing
Author Correction: A base editor for the long-term restoration of auditory function in mice with recessive profound deafness
Nature Biomedical Engineering, Published online: 07 September 2026; doi:10.1038/s41551-026-01794-5
Author Correction: A base editor for the long-term restoration of auditory function in mice with recessive profound deafnessCityPlanner: A Sandbox Agent for Executable Urban Planning
LightNav-0: Eliciting VLM Spatial Intelligence for Generalist Embodied Navigation
PRISM-Bench: An Audio-Centric Diagnostic Benchmark for Text-to-Audio-Video Generation
JT-SAFE-V2: Safety-by-Design Foundation Model with World-Context Data
Parameter Efficient Multi-Class Intelligent Scheduling for Multimodal Online Distributed Industrial Anomaly Detection
NSR-Boost: A Neuro-Symbolic Residual Boosting Framework for Industrial Legacy Models
SkillOpt: Executive Strategy for Self-Evolving Agent Skills
VILAS: A VLA-Integrated Low-cost Architecture with Soft Grasping for Robotic Manipulation
Break the Brake, Not the Wheel: Untargeted Jailbreak via Entropy Maximization
BacktestBench: Benchmarking Large Language Models for Automated Quantitative Strategy Backtesting
Simply Stabilizing the Loop via Fully Looped Transformer
Unlocking the Future of Hepatocellular Carcinoma Early Diagnosis: The Promise of Extracellular Vesicle Biomarkers
J Clin Transl Hepatol. 2026 Apr 28;14(4):462-477. doi: 10.14218/JCTH.2025.00589. Epub 2026 Apr 8.
ABSTRACT
Hepatocellular carcinoma (HCC) is one of the most prevalent and aggressive malignant tumors globally, with a notably low five-year survival rate. Its high mortality is largely attributed to challenges in early detection. Extracellular vesicles (EVs) are naturally occurring nanoparticles secreted by nearly all cell types and carry a diverse array of bioactive molecules, including proteins, nucleic acids (particularly non-coding RNAs), and lipids. EVs play pivotal roles in remodeling the tumor microenvironment and driving cancer progression through intercellular communication. Accumulating evidence has established that EVs are critically involved in the pathogenesis of HCC and are emerging as promising biomarkers for its early detection. With advances in EV isolation technologies, these vesicles have garnered considerable attention in the field of liquid biopsy for HCC. This review provides a comprehensive overview of the diagnostic potential of EV-derived biomarkers in HCC, including DNA, RNA, proteins, and lipids. Additionally, it discusses the advantages of integrating multi-omics approaches for HCC diagnosis. Furthermore, the review highlights the technical challenges in EV isolation and characterization, as well as the crucial role of reference genes in the standardization of EV data. These insights underscore the potential of EVs as novel, minimally invasive liquid biopsy biomarkers for the early diagnosis of HCC.
PMID:42181837 | PMC:PMC13195390 | DOI:10.14218/JCTH.2025.00589
Multi-omics integration identifies ribosome biogenesis-active macrophage subpopulation and its key gene GNL2 in driving liver hepatocellular carcinoma progression and mechanisms
Cancer Cell Int. 2026 May 14. doi: 10.1186/s12935-026-04330-2. Online ahead of print.
ABSTRACT
BACKGROUND: Liver hepatocellular carcinoma (LIHC) is a common malignancy, yet the core genes driving its progression and potential therapeutic targets remain insufficiently explored. Ribosome biogenesis (RB) is a critical biological process linked to various cancers; however, its systematic role in LIHC remains unclear.
METHODS: This study integrated LIHC single-cell RNA-Seq, bulk RNA-Seq, and spatial transcriptomic data with ribosome biogenesis-related gene sets to construct a single-cell atlas of LIHC. Weighted Gene Co-expression Network Analysis (WGCNA) was employed to characterize myeloid cell subsets. Furthermore, an LIHC prognostic risk model based on RB-related genes was developed using 117 machine-learning algorithm combinations. Key findings were subsequently corroborated through experimental validation and clinical sample analysis.
RESULTS: We identified a distinct macrophage subpopulation with high ribosome biogenesis activity, termed ribosome biogenesis-active macrophages (RAMs). These cells exhibited strong communication with inflammatory macrophages, potentially mediated by MIF-related receptor-ligand interactions. We further constructed an 8-gene prognostic model (PA2G4, GNL2, PWP1, DDX49, NOC4L, GDI2, CST7, and RCL1), which showed good predictive performance. Drug sensitivity analysis suggested that the high-risk group may be more responsive to several agents, including docetaxel. Among these genes, GNL2 was selected for further investigation. Elevated GNL2 expression was associated with increased stemness features in myeloid cells. Molecular docking analysis identified several candidate compounds with potential binding affinity to GNL2. Functionally, GNL2 knockdown in macrophages reduced TGF-β and TNF-α expression and was associated with decreased proliferation, migration, and invasion of LIHC cells.
CONCLUSION: We identified a highly active ribosome biogenesis-macrophage subpopulation (RAM), and constructed a robust risk model to aid in the diagnosis, prognosis, and treatment of LIHC. GNL2 is associated with increased expression of TGF-β and TNF-α and may contribute to LIHC progression.
PMID:42135716 | DOI:10.1186/s12935-026-04330-2