Genome sequencing of HCC from a Chinese cohort
Ontology highlight
ABSTRACT:
PROVIDER: EGAS00001001783 | EGA |
REPOSITORIES: EGA
Similar Datasets
Project description:Global expression profiling of miRNAs in liver tissue of HBV infected HCC and chronic hepatitis B (CHB) with no fibrosis was evaluated. A total of 40 differentially expressed miRNAs were identified in HCC. Top 10 miRNAs are validated in more numbers of HCC tisuues by qRT PCR. Finally six miRNAs (miR-15a, miR-16, miR-21,miR-29b-3p, miR-126, miR-142-3p, miR-193a-5p) showed similar expression pattern in both microarray and qRT PCR Differential expression analysis of microRNAs in HBV infected HCC (n=4) compared to CHB patients with no fibrosis (n=8) as control.
2015-04-15 | E-GEOD-67882 | biostudies-arrayexpress
Project description:miRNA played an important role in the process of carcinogenesis in HBV related hepatocellular carcinoma. Therefore, we performed miRNA microarray to evaluate the miRNAs that expressed differentially between HCC tumor versus non-tumor liver tissues. RNA was extracted from snap fresh tissue collected from resected HCC tumor and adjacent non-tumor liver tissues. All HCC tumors were HBV-associated HCC.
2015-07-22 | E-GEOD-69580 | biostudies-arrayexpress
Project description:Paraffin-embedded paired tumor and peri-carcinoma tissues (n=4) were obtained from the Biorepository of Fudan University Institute of Liver Cancer, which were used for the Affymetrix microarray analysis To investigate the progression of NASH to HCC, we established a differential gene expression profile by analyzing significant expression changes in pathologically confirmed NASH-HCC and peri-carcinoma specimens using Affymetrix microarrays.
2020-06-01 | GSE99807 | GEO
Project description:RNA-seq is a powerful tool for comprehensive characterization of whole transcriptome at both gene and exon levels and with a unique ability of identifying novel splicing variants. To date, RNA-seq analysis of HBV-related HCC has not been reported. In this study, we performed transcriptome analyses for 10 matched pairs of cancer and non-cancerous tissues from Chinese HBV-related hepatocelluar carcinoma patients using 36bp single-end sequencing approach on Solexa/Illumina GAII platform. On average, about 21.6 million sequencing reads and 10.6 million aligned reads were obtained for samples sequenced on each lane, which was able to identify > 50% of all the annotated genes for each sample. Furthermore, from by far the largest database of transcripts expressed in HCC tissues, we identified 1,378 significantly differently expressed genes (DEGs) and 24, 338 differentially expressed exons (DEEs). Comprehensive function analyses indicated that cell growth-related, metabolism-related and immune-related pathways were most significantly enriched by DEGs, pointing to a complex mechanism for HCC carcinogenesis. Positional gene enrichment analysis showed that DEGs were most significantly enriched at chromosome 8q21.3-24.3. The most interesting findings were from the analysis at exon levels where we characterized three major patterns of expression changes between gene levels and exon levels, implying a much complex landscape of transcript-specific differential expressions in HCC. Finally, we identified a novel highly up-regulated exon-exon junction in ATAD2 (ATPase family, AAA domain containing 2) gene in HCC tissues. Overall, to our best knowledge, our study represents the most comprehensive characterization of the HBV-related HCC transcriptome including exon level expression changes and novel splicing variants, which illustrated the power of RNA-seq and provided important clues for understanding the molecular mechanisms of HCC pathogenesis at system-wide levels. A comprehensive analysis of transcriptome for 10 match-paired HBV-related Chinese HCC and non-cancerous adjacent tissues. Processed data files: Exon-level results, gene-level results, differentially expressed exons, and differently expressed genes (DEGs).
2013-11-24 | E-GEOD-25599 | biostudies-arrayexpress
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.
2015-03-31 | E-GEOD-65485 | biostudies-arrayexpress
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.
2015-03-31 | GSE65485 | GEO
Project description:61 human HCCs were analyzed for genome-wide gene expression. Samples were collected at two sites in Germany, Heidelberg (HD) and Hannover (N). The Heidelberg Collection include 40 independent HCC: 19 liver resections and 17 explant liver specimen (4 not determined); median age at surgery was 57 years (range, 16-78), and the male/female ratio was 3:1. All diagnoses were confirmed by histological reevaluation, and use of the samples was approved by the local ethics committee. From 3 patients, two HCC nodules were included that previously showed different aCGH, indicating independent tumor development (tagged by _2). The underlying etiologies were HBV (n=8), HCV (n=9), alcohol (n=14), cryptogenic (n=11), genetic hemochromatosis (n=3), and Alpha-1 antitrypsin deficiency (n=2). The Hannover Collection include 21 HCC (HCC-Grad: G1-G3). Technical replicates were tagged with _B or _C differential genes expression in HCC liver (n=61) compared to control group (cell lines, n=3; normal liver tissue(NL), n=7). Technical replicates are indicated by _2.
2013-09-05 | E-GEOD-50579 | biostudies-arrayexpress
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.
2018-03-01 | GSE94660 | GEO
Project description:A comprehensive screening of site-specific N-glycopeptides in serum haptoglobin (Hp), a reporter molecule for aberrant glycosylation in HCC, has been performed to characterize glycopeptide markers for NASH-related HCCs.
2020-05-22 | PXD018502 | Pride
Project description:Non-alcoholic fatty liver disease/steatohepatitis (NAFLD/NASH) is a significant risk factor for hepatocellular carcinoma (HCC). However, a preclinical model of progressive NAFLD/NASH is largely lacking. Here, we report that mice with hepatocyte-specific deletion of Tid1, encoding a mitochondrial cochaperone, tended to develop NASH-dependent HCC. Mice with hepatic Tid1 deficiency showed impairing mitochondrial function and causing fatty acid metabolic dysregulation; meanwhile, sequentially developed fatty liver, NASH, and cirrhosis/HCC in a diethylnitrosamine (DEN) induced oxidative environment. The pathological signatures of human NASH, including cholesterol accumulation and activation of inflammatory and apoptotic signaling pathways, are also present in these mice. Clinically, low Tid1 expression was associated with unfavorable prognosis in patients with HCC. Empirically, hepatic Tid1 deficiency directly disrupts entire mitochondria that play a key role in the NASH-dependent HCC development. Overall, we established a new mouse model that develops NASH-dependent HCC and provides a promising approach to improve the treatment.
2022-06-02 | E-MTAB-9973 | biostudies-arrayexpress