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cs.AI, q-bio.NC updates on arXiv.org
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JT-SAFE-V2: Safety-by-Design Foundation Model with World-Context Data
arXiv:2605.24414v1 Announce Type: new Abstract: We introduce JT-Safe-V2, a large language model designed to advance the safety and trustworthiness of foundation models, extending our previous JT-Safe model toward a more comprehensive safety-by-design paradigm. JT-Safe-V2 emphasizes the joint optimization of general intelligence and safety-by-design through several key innovations: enriching pre-training data with contextual world knowledge, high-certainty pre-training procedures, and safety str
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cs.AI, q-bio.NC updates on arXiv.org
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SkillOpt: Executive Strategy for Self-Evolving Agent Skills
arXiv:2605.23904v2 Announce Type: replace Abstract: Agent skills today are hand-crafted, generated one-shot, or evolved through loosely controlled self-revision, none of which behaves like a deep-learning optimizer for the skill, and none of which reliably improves over its starting point under feedback. We argue the skill should instead be trained as the external state of a frozen agent, with the same discipline that makes weight-space optimization reproducible. SkillOpt is, to our knowledge,
SkillOpt: Executive Strategy for Self-Evolving Agent Skills
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Omics in Hepatocellular
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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.ABSTRACTBACKGROUND: 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 tra
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