Comparison of expression microarray data and somatic mutation signature in primary HCC
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE36390 | GEO | 2012/03/10
SECONDARY ACCESSION(S): PRJNA153277
REPOSITORIES: GEO
Similar Datasets
Project description:Hepatocellular carcinoma (HCC) is the third leading cause of cancer-related death worldwide. We sequenced and analyzed the whole genomes of primary HCCs. To examine the influence of transcription-coupled repair (TCR) on somatic substitution patterns in HCC, we performed expression microarrays analysis and compared gene expression levels and the number of substitutions in 7 HCCs. Seven primary HCC were analyzed and compared with somatic substituion numbers.
2012-03-10 | E-GEOD-36390 | biostudies-arrayexpress
Project description:We used array-based comparative genomic hybridization (arrayCGH) of 76 hepatocellular carcinomas (HCCs) to search for genetically disrupted genes. Seventy-six HCC clinical specimens were analyzed. Genomic DNA of the tumor sample was labeled with Cy5 and reference normal DNA (Promega) was labeled with Cy3.
2012-01-20 | E-GEOD-14322 | biostudies-arrayexpress
Project description:<p>The ncRNA transcriptome of human hepatocellular carcinoma (HCC) is largely unexplored. We used CAGE to characterize transcription start sites across different etiologies of human HCCs with emphasis on ncRNAs. Here we report that retroviral LTR promoters, expressed in healthy tissues such as testis and placenta but not liver, are widely activated in HCC. Despite HCC heterogeneity, a subset of LTR-derived ncRNAs were more than 10-fold up-regulated in the vast majority of samples. HCCs with a high LTR activity mostly had a viral etiology, were less differentiated and showed higher risk of recurrence. CAGE enabled us to build a promoter map for HCC, which uncovers a new layer of complexity in HCC genomics.</p>
| phs000885 | dbGaP
Project description:p53 suppresses tumor progression and metastasis by regulating a large set of genes and microRNAs. By profiling 92 primary hepatocellular carcinomas (HCCs) and 9 HCC cell lines, we found that p53 upregulates microRNAs including miR-200 and miR-192 family members. By sequencing TP53 in 92 HCC samples, we classified the 92 samples into two groups (wt and mut). We also classified 9 HCC cell lines by testing p21 expression after DNA-damage mediated p53 activation. We then profiled microRNA expression in 92 HCC tissue samples and 9 HCC celll lines to identify p53-regulated microRNAs.
2011-05-11 | E-GEOD-28661 | biostudies-arrayexpress
Project description:p53 suppresses tumor progression and metastasis by regulating a large set of genes and microRNAs. By profiling 92 primary hepatocellular carcinomas (HCCs) and 9 HCC cell lines, we found that p53 upregulates microRNAs including miR-200 and miR-192 family members.
2011-05-11 | GSE28661 | GEO
Project description:A mouse model of HCC has been developed based on the reported inactivation of the RB pathway in the majority of human HCC. This mouse model harbors floxed alleles of Rb and p130 genes, as well as germline mutation of the p107 gene. Various strategies to activate the activity of a Cre recombinase leads to the efficient deletion of the three genes in the liver of adult mice (TKO mice). Disruption of the RB pathway induces the rapid development of HCC. These HCCs share many similar features of human HCC. The goal of this array is to assess genome wide expression of TKO HCCs. Gene expression of control livers (n=4) or TKO HCCs (n=5) was measured using the Affymetrix GeneChip Mouse Genome 430-2.0 arrays
2010-07-30 | E-GEOD-19004 | biostudies-arrayexpress
Project description:Sex differences in hepatocellular carcinoma (HCC) development are regulated by sex and non-sex chromosomes, sex hormones, and environmental factors. We previously reported that Ncoa5+/- mice develop HCC in a male-biased manner. Here we show that NCOA5 expression was reduced in male patient HCCs while the expression of an NCOA5-interacting tumor suppressor, TIP30, was lower in female HCCs. Tip30 heterozygous deletion did not change HCC incidence in Ncoa5+/- male mice but dramatically increased HCC incidence in Ncoa5+/- female mice, accompanied by hepatic hyperpolarization-activated cyclic nucleotide-gated cation channel 3 (HCN3) overexpression. HCN3 overexpression cooperated with MYC to promote mouse HCC development, whereas Hcn3 knockout preferentially hindered HCC development in female mice. Furthermore, HCN3 amplification and overexpression occurred in human HCCs and correlated with a poorer prognosis of patients in a female-biased manner. Our results suggest that TIP30 and NCOA5 protect against female liver oncogenesis and that HCN3 is a female-biased HCC driver.
2023-08-29 | GSE228531 | GEO
Project description:The diethylnitrosamine HCC rat model (DEN-HCC) is a useful preclinical model mirroring human hepatocellular carcinoma. To overcome tumor heterogeneity of human HCCs linked to different etiologies and clonal selection, rat HCC samples were compared with matched non-tumor livers in order to identify HCC-related genes involved in the carcinogenetic process. Specifically, male Wistar rats received DEN (Sigma-Aldrich) in the drinking water (100 mg/L) for 8 weeks. Two weeks later the end of DEN treatment, animals were monitored by ultrasound imaging. Animals were euthanized 1 or 2 months after the end of DEN treatment, when the major diameter of at least one HCC nodule reached a dimension of 10 mm. Samples were collected for molecular biology and total RNA for microarray analysis was extracted by using Trizol. Two rat livers from untreated mice were included in the analysis.
2023-05-23 | E-MTAB-11977 | biostudies-arrayexpress
Project description:siRNA-mediated inhibition compared to untreated cells and cells transfected with nonsense siRNA Together with far upstream element binding protein (FBP), the FBP-interacting repressor (FIR) represents a molecular tool for the transcriptional fine tune regulation of target genes. Previous evidence indicates that strong overexpression of FBP in human hepatocellular carcinoma (HCC) supports tumor growth and correlates with poor patient prognosis. However, the role of the transcriptional repressor FIR in hepatocarcinogenesis remains poorly delineated. We show that overexpression of FIR correlates with tumor dedifferentiation and tumor cell proliferation in about 60% of primary HCCs. Elevated FIR levels are associated with genomic gains of the fir gene locus at chromosome 8q24.3 in human HCC specimens. In vitro, nuclear enrichment of FIR supports HCC cell proliferation and migration. Expression profiling of HCC cells after siRNA-mediated silencing of FIR identified the transcription factor DP-1 (TFDP1) as a transcriptional target of FIR. Surprisingly, FIR stimulates the expression of FBP in a TFDP1/E2F-dependent manner. FIR splice variants lacking or containing exon 2 and/or exon 5 are expressed in the majority of HCCs. Specific inhibition of FIR isoforms with and without exon 2 revealed that all FIR splice variants facilitate tumor-supporting effects. This finding was confirmed in xenograft transplantation experiments with lentiviral-infected shRNA targeting all FIR variants as well as FIR with and without exon 2. In summary, high-level nuclear FIR does not facilitate repressor properties but supports tumor growth in HCC cells. Thus, the pharmacological inhibition of FIR might represent a promising therapeutic strategy for HCC patients. Expression profiling of cells transfected with scrambled/nonsense siRNA (control), and after siRNA-mediated FIR inhibition.
2014-09-03 | E-GEOD-55692 | biostudies-arrayexpress
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