Single-cell transcriptomics reveals etiology-specific T-cell heterogeneity in hepatocellular carcinoma and implicates regulatory
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE319709 | GEO | 2026/02/20
REPOSITORIES: GEO
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2008-09-11 | GSE12723 | GEO
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2013-11-14 | E-GEOD-44074 | biostudies-arrayexpress
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Project description:Hepatocellular carcinoma (HCC) is a leading cause of cancer-related death worldwide, with chronic hepatitis B virus (HBV) infection being a major contributor to its development. Despite this, effective treatment for HBV-associated HCC remains a significant challenge. In this study, we combined the strengths of vesicular stomatitis virus (VSV) and therapeutic vaccines to propose a novel strategy for treating HBV-related liver cancer. We engineered an oncolytic virus that delivers hepatitis B surface antigen (HBsAg) and the IL-15 cytokine directly to tumor cells, thereby enhancing immune activation and promoting tumor cell destruction. As the tumor cells die, they release additional virus particles, spreading HBsAg and IL-15 expression to neighboring tumor cells. This approach demonstrated promising efficacy in multiple HBV-positive HCC mouse models.
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Project description:We applied small RNA Solexa sequencing technology to identify microRNA expression in human liver samples from surgically removed liver tissues including three normal liver tissues (distal normal liver tissue of liver hemangioma), an hepatitis B virus (HBV)-infected liver, a severe chronic hepatitis B liver, two HBV-related hepatocellular carcinoma (HCC), an hepatitis C virus (HCV)-related HCC, and an HCC without HBV or HCV infection. All samples were collected with the informed consent of the patients and the experiments were approved by the ethics committee of Second Military Medical University, Shanghai, China. We investigated the miRNome in human normal liver and suggested some deregulated abundantly expressed microRNAs in HCC. center_name: National Key Laboratory of Medical Immunology & Institute of Immunology, Second Military Medical University, Shanghai, China. Examination of miRNome in human liver samples from surgically removed liver tissues including three normal liver tissues (distal normal liver tissue of liver hemangioma), an hepatitis B virus (HBV)-infected liver tissue, a severe chronic hepatitis B liver tissue, an HBV-related hepatocellular carcinoma (HCC) tissue and adjacent liver tissues of different regions,an HBV-related HCC tissue and adjacent liver tissue, an hepatitis C virus (HCV)-related HCC tissue and adjacent liver tissue, and an HCC without HBV or HCV infection and adjacent liver tissue. All 15 human liver tissue samples.
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2026-02-11 | GSE318726 | GEO
Project description:Metabolic dysfunction–associated steatohepatitis (MASH) is a rapidly growing cause of hepatocellular carcinoma (HCC) and is associated with poor clinical outcomes and limited responsiveness to immune checkpoint inhibitors. Emerging evidence suggests that immune dysregulation within the tumor microenvironment contributes to disease progression; however, the transcriptional programs distinguishing MASH-associated HCC from non-MASH HCC remain incompletely characterized. To address this gap, we performed bulk RNA sequencing on total RNA isolated from MASH and non-MASH tumor tissues. This dataset was generated to enable comparative transcriptomic analysis of tumor-intrinsic and immune-related pathways associated with MASH-driven hepatocarcinogenesis, with particular relevance to immune organization, metabolic stress responses, and tumor–immune interactions.The resulting RNA-seq data provide a resource for investigating alterations in immune cell–associated gene signatures, metabolic pathways, and microenvironmental features that may underlie immune dysfunction in MASH-HCC.
2026-02-11 | GSE318724 | GEO
Project description:Background & Aims: Chronic HBV patients with concomitant metabolic dysfunction-associated steatohepatitis (MASH) have been shown to develop more advanced fibrosis faster with more severe liver disease as compared to patients with chronic HBV alone. However, our understanding of the underlying mechanisms is limited. Here we study how MASH co-morbidity impact immune activity in the liver of patients with chronic HBV infection. Methods: Bulk RNA sequencing was performed on liver biopsies from patients with only MASH (n=10), only HBeAg-negative chronic HBV (ENEG; n=11), combined MASH/ENEG (n=9) and healthy controls (n=9). Biopsies with no or minimal fibrosis (≤F2) were selected to avoid confounding effects of fibrosis. We compared whole transcriptome data from patients with MASH/ENEG to those with ENEG alone to determine the impact of MASH co-morbidity on chronic hepatitis B. Results: There is a high degree of overlap of liver gene expression profiles in patients with only ENEG versus those with only MASH compared to healthy controls, suggesting a largely shared mechanism of liver dysfunction and immune activity for these distinct conditions. In patients with ENEG, MASH co-morbidity significantly reduced interferon pathway activity (NES=2.03, p.adj=0.0251), the expression of ISGs (e.g., IFIT2, IFI27, IFITM1, IFI6), and macrophage gene signatures (e.g., MARCO, CD163, CD5L, CD63), when compared to patients with ENEG alone. Conclusions: Transcriptomic profiling of the liver suggests that MASH negatively impacts ISGs expression in the liver of patients with ENEG, which may affect antiviral immune pathways, viral replication and inflammatory responses resulting in an increased risk of advanced fibrosis in patients with chronic hepatitis B. Our study provides valuable insights for guiding future research aimed at developing effective, tailored strategies for managing patients with both conditions.
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2016-06-30 | E-MTAB-4809 | biostudies-arrayexpress
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