Decoding Tumor–Immune Interactions in Hepatocellular Carcinoma Through Network-Centered Identification of CXCR2

Seven-Gene Signature and Immune Microenvironment as Determinants of Survival Rate in Colorectal Carcinoma

A seven-gene immune-related prognostic signature that, combined with clinicopathological parameters, provides a robust tool for individualized survival prediction and may guide precision management in CRC patients is developed and validated.

Integrated Transcriptomic Analyses Identify Four Prognosis-Associated Genes in Hepatocellular Carcinoma

Hepatocellular carcinoma (HCC) is one of the malignant tumors with high incidence and mortality rates worldwide. Given the poor prognosis of patients with HCC, it is crucial to explore the molecular mechanisms underlying HCC development and to evaluate prognostic markers. Differential expression analysis followed by univariate Cox, LASSO, and multivariate Cox regression identified four genes (EPO, SOCS2, IL18RAP, and KPNA2), and a Cox-based risk score was evaluated in the TCGA-LIHC cohort and externally in GSE14520 using Kaplan–Meier and time-dependent ROC analyses. Bulk, single-cell, and protein resources provided convergent expression context. Survival machine-learning analysis using observed overall-survival time and censoring status identified Cox–Ridge as the best-performing model in TCGA-LIHC, with more modest performance in GSE14520, and immune profiling revealed risk-group-associated differences in estimated immune and stromal components, immune-cell composition, and immune-checkpoint expression. The oncoPredict/GDSC2 screen highlighted five potential drug candidates for experimental prioritization. Because the drug screen is based on computationally predicted sensitivities, these findings should be regarded as hypothesis-generating and require validation in prospective cohorts and experimental systems before clinical translation.

Researching the role of ubiquitination and macrophage activation-related genes in hepatocellular carcinoma through a systematic study based on gene expression profiling.

The findings lay the groundwork for precision oncology paradigms, facilitating the translational trajectory of these targets to optimize clinical prognosis, and underscores the potential of UMARGs in advancing HCC treatment strategies and improving patient outcomes.

Identification of a metastasis-associated prognostic gene signature in osteosarcoma through integrated bioinformatics and functional analysis

Single-cell transcriptome atlas identified ERO1A+ angiogenesis-associated macrophage with a central potential in promoting hepatocellular carcinoma

Hepatocellular carcinoma (HCC) is the most prevalent form of liver cancer and remains a global health challenge due to its complexity and limited therapeutic options. Within the HCC tumor microenvironment, tumor-associated macrophages (TAMs) are the most abundant immune cells and critical mediators of immunosuppression and angiogenesis, but their heterogeneity and clinical relevance remain incompletely characterized. In this study, we investigated TAMs in clinical HCC by integrative analysis of single-cell RNA-sequencing (scRNA-seq) data from 46 HCC and 13 adjacent liver samples across five independent cohorts (256,236 cells). The resulting unified macrophage atlas identified eight subsets based on functional gene modules, with monocyte-derived angiogenesis-associated macrophages (Angio-Mac) emerging as the most clinically significant subset. Crucially, the identification of this cluster was robustly reproduced by a cross-platform validation using an independent human HCC single-nucleus RNA-sequencing (snRNA-seq) dataset and a sensitivity re-analysis with a strict 20% mitochondrial filtration cutoff. Angio-Mac expanded in advanced HCC, correlated with poor prognosis, and exhibited pro-tumorigenic transcriptomic features, including enhanced mTORC1 signaling and suppressed antigen presentation. Angio-Mac overexpressed SPP1 and was suggested to promote interactions with T/NK cells via the SPP1-CD44 axis. Unbiased risk analysis further revealed ERO1A as an Angio-Mac-specific marker linked to advanced HCC and poor prognosis. In contrast, Kupffer cell-derived TAMs displayed a “stalled” phenotype with limited pro-tumor activity. These findings highlight Angio-Mac as a macrophage subset in HCC characterized by prominent expression of genes associated with angiogenesis and immunosuppression. Consequently, this macrophage subset and its signature genes represent valuable candidates for further mechanistic investigation and clinical validation.

CDC20B Dysregulation: Links to Tumor Prognosis and Immunity.

OBJECTIVE This study aimed to clarify the pan-cancer expression pattern, upstream regulatory mechanisms, prognostic relevance, and immune associations of CDC20B. METHOD Using public databases (GTEx, GEO, and TCGA), we examined CDC20B expression and its associations with prognosis and tumor immunity across multiple cancers. Immunohistochemistry (IHC) on an independent clinical cohort was performed to validate CDC20B upregulation in tumor tissues. Promoter methylation, genetic alterations, and immune infiltration were analyzed using bioinformatics tools (cBioPortal, UALCAN, TIMER2.0, ESTIMATE). Functional enrichment was assessed by GSEA and single-cell state analysis (CancerSEA). RESULTS CDC20B was markedly upregulated in most tumor types (p < 0.001), with strong diagnostic efficiency (AUC > 0.7 in 15 cancers) and potential regulation by promoter hypomethylation. IHC confirmed its overexpression in clinical tumor tissues. However, the prognostic impact of CDC20B was cancer-type-specific: high expression correlated with poor overall survival in UCS, LGG, KIRC, and OV, but with favorable survival in BRCA, LUAD, and PAAD. CDC20B expression was associated with immune infiltration patterns, showing negative correlations with ImmuneScore in most cancers but positive correlations with CD8+ T cells in PAAD. Functional analyses indicated involvement in EMT, KRAS/NF-κB signaling, and DNA damage response pathways. DISCUSSION The dual prognostic role of CDC20B suggests context-dependent functions, likely influenced by tumor microenvironment composition and underlying oncogenic programs. Promoter hypomethylation emerges as a potential epigenetic driver of overexpression. The associations with immune modulation and genomic instability suggest that CDC20B is a candidate biomarker, though causal relationships require experimental validation. CONCLUSION CDC20B may contribute to tumor progression in a context-dependent manner, with its prognostic impact varying across cancer types. Its role in tumor immunity and oncogenic pathways warrants further investigation, particularly in stratified patient populations.