Project description:To investigate the transcriptomic analysis of HBV-KMT2B integrated HCC, RNA-seq analysis of tumor tissue of HBV-KMT2B integrated HCC was performed. To further analyze KMT2B integrations, we identified full-length complementary DNA by long-read RNA-seq (Iso-seq).
Project description:To investigate the transcriptomic analysis of HBV-KMT2B integrated HCC, RNA-seq analysis of tumor tissue of HBV-KMT2B integrated HCC was performed. To further analyze KMT2B integrations, we identified full-length complementary DNA by long-read RNA-seq (Iso-seq).
Project description:We identified full-length complementary DNA by long-read RNA-seq (Iso-seq) in HBV-KMT2B integrated HCC sample. To compare the data of HCC sapmle with HBV-KMT2B integrated HPCs, which reproduces the sequence of the HCC sample, we performed long-read RNA-seq in HBV-KMT2B integrated HPCs, as well.
Project description:To investigate the global analysis of H3K4me3 of HBV-KMT2B integrated HPCs, CUT&Tag analysis of HBV-KMT2B integrated HPCs and KMT2B heterozygous knockout HPCs was performed.
Project description:Purpose: To gain molecular insights of HBV integration that may contribute to HCC tumorigenesis, we performed whole transcriptome sequencing and whole genome copy number profiling of hepatocellular carcinoma (HCC) samples from 50 Chinese patients. Results: We identified a total of 33 HBV-human integration sites in 16 of 44 HBV-positive HCC tissues, which were enriched in HBV genotype C-infected patients. In addition, significantly recurrent HBV-MLL4 integration (18%). This dataset is part of the TransQST collection.
Project description:RNA-seq analysis of hepatocellular carcinoma (HCC), in which HBV-KMT2B integration was identified. The tumor region and nontumorous region were extracted from the HCC surgical specimen.
Project description:Iso-seq analysis of hepatocellular carcinoma (HCC), in which HBV-KMT2B integration was identified. The tumor region and nontumorous region were extracted from the HCC surgical specimen.
Project description:Purpose: To gain molecular insights of HBV integration that may contribute to HCC tumorigenesis, we performed whole transcriptome sequencing and whole genome copy number profiling of hepatocellular carcinoma (HCC) samples from 50 Chinese patients. Results: We identified a total of 33 HBV-human integration sites in 16 of 44 HBV-positive HCC tissues, which were enriched in HBV genotype C-infected patients. In addition, significantly recurrent HBV-MLL4 integration (18%; 8/44) was found in this cohort of patients. Conclusions: This is the first report on the molecular basis of the MLL4 integration driving MLL4 over-expression. HBV-MLL4 integration occurred frequently in Chinese HCC patients, representing a unique molecular segment for HCC with HBV infection.
Project description:Purpose: Chronic Hepatitis B virus (HBV) infection leads to liver fibrosis which is a major risk factor in Hepatocellular carcinoma (HCC) and an independent risk factor of recurrence after HCC tumor resection. HBV genome can be inserted into human genome, and chronic inflammation may trigger somatic mutations. Several studies characterized HBV integration sites in HCC patients with regard to frequently occurring hotspots. However, how HBV integration and other genomic changes contribute to the risk of tumor recurrence with regard to different degree of liver fibrosis is not clearly understood. In this study, we aim to find potential molecular mechanisms underlying tumor recurrence of HBV-associated HCC (HBV-HCC) with different degree of liver fibrosis. Methods: We performed RNA sequencing of 21 pairs of tumor and non-neoplastic liver tissues of HBV-HCC patients and performed comprehensive genomic analysis of our RNAseq data and public available sequencing data related to HBV-HCC. We developed a robust pipeline for sensitively identifying HBV integration sites based on sequencing data. Simulations with sequencing data showed that our method outperformed existing methods. We also compared SNPs of each sample with SNPs in cancer census database and inferred patient’s pathogenic SNP loads in tumor and non-neoplastic liver tissues. Conclusions: The HBV-integration and pathogenic SNP load patterns for HCC recurrence risk vary depending on liver fibrosis stage, suggesting potentially different tumorigenesis mechanisms for low and high liver fibrosis patients.