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FiberTune: Preserving Action-Fiber Visual Residuals in Vision-Language-Action Fine-Tuning
LightNav-0: Eliciting VLM Spatial Intelligence for Generalist Embodied Navigation
Integrative Multi-Omics Mendelian Randomization Analysis Identifies NIT2 as a Potential Metabolic Risk Gene in Hepatocellular Carcinoma
J Gene Med. 2026 Sep;28(9):e70111. doi: 10.1002/jgm.70111.
ABSTRACT
BACKGROUND: Metabolic pathways are crucial in hepatocellular carcinoma (HCC) pathogenesis, but causal metabolic genes remain unclear. This study used Summary data-based Mendelian Randomization (SMR) and colocalization to identify metabolism-related genetic loci influencing HCC risk.
METHODS: Differentially expressed genes in hepatic malignancy phenotype versus normal tissues from TCGA and GTEx were analyzed. Metabolism-related candidates were examined via SMR and colocalization using multi-omics data: methylation (mQTL), expression (eQTL), and protein (pQTL) quantitative trait loci.
RESULTS: Multi-omics integration identified NIT2 as a key metabolic regulator for HCC. The cg13016775 locus of NIT2 was associated with elevated HCC risk at gene (OR = 1.618, 95% CI: 1.199-2.182) and protein (OR = 4.432, 95% CI: 1.783-11.018) levels. Colocalization supported a shared causal variant (PPH4 > 0.6), linking NIT2 to hepatocarcinogenesis via metabolic regulation.
CONCLUSIONS: This study provides multi-omics evidence for NIT2 as a potential causal gene in HCC, enhancing understanding of metabolic contributions to HCC pathogenesis and highlighting integrative genomics for uncovering causal relationships.
PMID:42681890 | PMC:PMC13534973 | DOI:10.1002/jgm.70111
Claw-Anything: Benchmarking Always-On Personal Assistants with Broader Access to User's Digital World
MobileGym: A Verifiable and Highly Parallel Simulation Platform for Mobile GUI Agent Research
Agent World Model: Infinity Synthetic Environments for Agentic Reinforcement Learning
HiTeC: Hierarchical Contrastive Learning on Text-Attributed Hypergraph with Semantic-Aware Augmentation
Multi-omics analysis identified serum B4GALT1 as a prognostic factor for small cell lung cancer
J Thorac Dis. 2026 Apr 30;18(4):353. doi: 10.21037/jtd-2025-1-2610. Epub 2026 Mar 20.
ABSTRACT
BACKGROUND: Small cell lung cancer (SCLC) is an aggressive neuroendocrine tumor characterized by rapid progression, early metastasis, and high mortality, with limited effective long-term treatment options. B4GALT1, a β-1,4-galactosyltransferase, has been implicated in the malignant progression of various cancers, but its specific role and underlying mechanisms in SCLC remain largely unexplored. We conducted a multi-omics analysis and clinical sample study to explore the function of B4GALT1 in SCLC.
METHODS: This study comprehensively investigated the expression pattern, functional significance, and clinical relevance of B4GALT1 in SCLC. We conducted multi-omics analyses, including single-cell data processing, InferCNV analysis, and immune infiltration analysis, to explore the association between B4GALT1 and the immune microenvironment of SCLC and patient survival. To determine B4GALT1 as a potential circulating biomarker, quantitative data-independent acquisition (DIA) proteomics analysis was performed on serum samples from SCLC patients and healthy controls. Enzyme-linked immunosorbent assay (ELISA) was used to further verify the differential expression of serum B4GALT1 in a larger cohort of SCLC patients, to evaluate its diagnostic, prognostic, and treatment response predictive value.
RESULTS: Multi-omics analysis revealed that B4GALT1 expression was significantly associated with patient survival. The expression of B4GALT1 positively correlated with macrophage infiltration in the tumor and negatively correlated with CD4+ T cells in the tumor. There was a negative correlation in inactivated naïve B cells, eosinophils, and CD4 naïve T cells, while it showed a positive correlation in dendritic cells, M0/M1/M2 macrophages, natural killer (NK) cells, CD8 T cells, follicular helper T cells, and regulatory T cells. ELISA results showed that serum protein B4GALT1 expression was higher in patients with SCLC than in healthy controls. Elevated serum B4GALT1 protein levels correlated with poor treatment outcomes in patients with SCLC undergoing chemoradiotherapy.
CONCLUSIONS: Our findings establish B4GALT1 as a critical prognostic, diagnostic, and predictive biomarker in SCLC, with its expression closely linked to the tumor immune microenvironment and treatment response. Targeting B4GALT1 or its related pathways may represent a novel therapeutic strategy, and serum B4GALT1 holds promise as a liquid biopsy marker for SCLC patient stratification, monitoring, and guiding treatment decisions.
PMID:42182735 | PMC:PMC13190155 | DOI:10.21037/jtd-2025-1-2610
Multi-omics analysis identified serum B4GALT1 as a prognostic factor for small cell lung cancer
J Thorac Dis. 2026 Apr 30;18(4):353. doi: 10.21037/jtd-2025-1-2610. Epub 2026 Mar 20.
ABSTRACT
BACKGROUND: Small cell lung cancer (SCLC) is an aggressive neuroendocrine tumor characterized by rapid progression, early metastasis, and high mortality, with limited effective long-term treatment options. B4GALT1, a β-1,4-galactosyltransferase, has been implicated in the malignant progression of various cancers, but its specific role and underlying mechanisms in SCLC remain largely unexplored. We conducted a multi-omics analysis and clinical sample study to explore the function of B4GALT1 in SCLC.
METHODS: This study comprehensively investigated the expression pattern, functional significance, and clinical relevance of B4GALT1 in SCLC. We conducted multi-omics analyses, including single-cell data processing, InferCNV analysis, and immune infiltration analysis, to explore the association between B4GALT1 and the immune microenvironment of SCLC and patient survival. To determine B4GALT1 as a potential circulating biomarker, quantitative data-independent acquisition (DIA) proteomics analysis was performed on serum samples from SCLC patients and healthy controls. Enzyme-linked immunosorbent assay (ELISA) was used to further verify the differential expression of serum B4GALT1 in a larger cohort of SCLC patients, to evaluate its diagnostic, prognostic, and treatment response predictive value.
RESULTS: Multi-omics analysis revealed that B4GALT1 expression was significantly associated with patient survival. The expression of B4GALT1 positively correlated with macrophage infiltration in the tumor and negatively correlated with CD4+ T cells in the tumor. There was a negative correlation in inactivated naïve B cells, eosinophils, and CD4 naïve T cells, while it showed a positive correlation in dendritic cells, M0/M1/M2 macrophages, natural killer (NK) cells, CD8 T cells, follicular helper T cells, and regulatory T cells. ELISA results showed that serum protein B4GALT1 expression was higher in patients with SCLC than in healthy controls. Elevated serum B4GALT1 protein levels correlated with poor treatment outcomes in patients with SCLC undergoing chemoradiotherapy.
CONCLUSIONS: Our findings establish B4GALT1 as a critical prognostic, diagnostic, and predictive biomarker in SCLC, with its expression closely linked to the tumor immune microenvironment and treatment response. Targeting B4GALT1 or its related pathways may represent a novel therapeutic strategy, and serum B4GALT1 holds promise as a liquid biopsy marker for SCLC patient stratification, monitoring, and guiding treatment decisions.
PMID:42182735 | PMC:PMC13190155 | DOI:10.21037/jtd-2025-1-2610
RDFace: A Benchmark Dataset for Rare Disease Facial Image Analysis under Extreme Data Scarcity and Phenotype-Aware Synthetic Generation
TSPO: Breaking the Double Homogenization Dilemma in Multi-turn Search Policy Optimization
Vision-as-Inverse-Graphics Agent via Interleaved Multimodal Reasoning
Integrative Multi-Omics and Single-Cell Analysis Reveal THOC3 and THOC7 as Oncogenic RNA Processing Regulators in Lung Adenocarcinoma
Int J Med Sci. 2026 Mar 9;23(4):1408-1430. doi: 10.7150/ijms.128975. eCollection 2026.
ABSTRACT
Lung adenocarcinoma (LUAD) remains a leading cause of cancer-related mortality worldwide. Although the transcription-export (TREX) complex plays a central role in RNA maturation and nuclear export, the clinical and biological relevance of individual THO Complex Subunit (including THOC1, THOC2, THOC3, THOC5, THOC6, and THOC7) in LUAD is not well defined. We performed integrative analyses combining bulk transcriptomics from TCGA/GTEx and independent GEO cohorts, survival modeling, DNA methylation profiling, protein-level annotation from public resources, protein-protein interaction network analysis, immune infiltration estimation (TIMER), and single-cell RNA sequencing (scRNA-seq) to evaluate the relevance of THOC3 and THOC7 in LUAD. Across TCGA and external GEO validation datasets, THOC3 and THOC7 were consistently upregulated in LUAD and associated with poorer overall and disease-free survival, whereas other THO complex members showed weaker or inconsistent associations. Given these comparatively consistent and reproducible signals, we therefore prioritized THOC3 and THOC7 for downstream multi-layer analyses. Epigenetic profiling and interaction network analyses placed both genes within conserved RNA processing and export programs linked to genome maintenance pathways. Single-cell transcriptomic analysis provided additional resolution, demonstrating predominant enrichment of THOC3 and THOC7 in malignant epithelial clusters, with THOC3 aligning with transcriptional programs associated with DNA replication and repair, and THOC7 with proliferative and checkpoint-related states. Notably, expression of both genes was also detectable in myeloid and neutrophil subsets, and THOC7 expression remained elevated in recurrent LUAD samples, indicating association with aggressive and treatment-resistant disease states. Collectively, by integrating bulk, single-cell, epigenetic, and immune profiling across multiple independent cohorts, this study identifies THOC3 and THOC7 as reproducible molecular correlates of aggressive LUAD phenotypes. These highlight dysregulated RNA export programs as potential biomarkers of poor prognosis and motivate future functional studies to assess RNA export dependencies in LUAD.
PMID:41938520 | PMC:PMC13048885 | DOI:10.7150/ijms.128975
Integrative Multi-Omics and Single-Cell Analysis Reveal THOC3 and THOC7 as Oncogenic RNA Processing Regulators in Lung Adenocarcinoma
Int J Med Sci. 2026 Mar 9;23(4):1408-1430. doi: 10.7150/ijms.128975. eCollection 2026.
ABSTRACT
Lung adenocarcinoma (LUAD) remains a leading cause of cancer-related mortality worldwide. Although the transcription-export (TREX) complex plays a central role in RNA maturation and nuclear export, the clinical and biological relevance of individual THO Complex Subunit (including THOC1, THOC2, THOC3, THOC5, THOC6, and THOC7) in LUAD is not well defined. We performed integrative analyses combining bulk transcriptomics from TCGA/GTEx and independent GEO cohorts, survival modeling, DNA methylation profiling, protein-level annotation from public resources, protein-protein interaction network analysis, immune infiltration estimation (TIMER), and single-cell RNA sequencing (scRNA-seq) to evaluate the relevance of THOC3 and THOC7 in LUAD. Across TCGA and external GEO validation datasets, THOC3 and THOC7 were consistently upregulated in LUAD and associated with poorer overall and disease-free survival, whereas other THO complex members showed weaker or inconsistent associations. Given these comparatively consistent and reproducible signals, we therefore prioritized THOC3 and THOC7 for downstream multi-layer analyses. Epigenetic profiling and interaction network analyses placed both genes within conserved RNA processing and export programs linked to genome maintenance pathways. Single-cell transcriptomic analysis provided additional resolution, demonstrating predominant enrichment of THOC3 and THOC7 in malignant epithelial clusters, with THOC3 aligning with transcriptional programs associated with DNA replication and repair, and THOC7 with proliferative and checkpoint-related states. Notably, expression of both genes was also detectable in myeloid and neutrophil subsets, and THOC7 expression remained elevated in recurrent LUAD samples, indicating association with aggressive and treatment-resistant disease states. Collectively, by integrating bulk, single-cell, epigenetic, and immune profiling across multiple independent cohorts, this study identifies THOC3 and THOC7 as reproducible molecular correlates of aggressive LUAD phenotypes. These highlight dysregulated RNA export programs as potential biomarkers of poor prognosis and motivate future functional studies to assess RNA export dependencies in LUAD.
PMID:41938520 | PMC:PMC13048885 | DOI:10.7150/ijms.128975
User-preference alignment with uncertainty-aware interactive rectification for liver organ and tumor segmentation and analysis from CT images
npj Digital Medicine, Published online: 03 April 2026; doi:10.1038/s41746-026-02544-2
User-preference alignment with uncertainty-aware interactive rectification for liver organ and tumor segmentation and analysis from CT imagesX-World: Controllable Ego-Centric Multi-Camera World Models for Scalable End-to-End Driving
Author Correction: Signatures of ambient pressure superconductivity in thin film La<sub>3</sub>Ni<sub>2</sub>O<sub>7</sub>
Nature, Published online: 31 March 2026; doi:10.1038/s41586-026-10335-8
Author Correction: Signatures of ambient pressure superconductivity in thin film La3Ni2O7