Hepatocellular carcinoma vs. corresponding noncancerous liver or normal liver
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE4108 | GEO | 2009/01/06
SECONDARY ACCESSION(S): PRJNA95273
REPOSITORIES: GEO
Similar Datasets
Project description:Hepatocellular carcinoma (HCC) remains a major health problem worldwide, and HCC patients have a poor prognostic outcome. In this study, we systematically disclose mechanisms of hepatocarcinogenesis, and also effectively identify and validate novel anticancer targets in HCCs. Keywords: disease state analysis total 58 cDNA microarrays, all experiment samples are hepatocellular carcinoma. RNAs from 33 corresponding noncancerous livers and 5 normal livers were used as the reference, respectively. The tumor samples were labeled with Cy5-dUTP.The nontumor samples were labeled with Cy3-dUTP.
2009-01-06 | E-GEOD-4108 | biostudies-arrayexpress
Project description: Not available
| S-DIXA-D-1138 | biostudies-other
Project description:Background & Aims: The recurrence determines the postoperative prognosis of patients with hepatocellular carcinoma (HCC). It is unknown whether de novo HCCs derive from the liver with disability of an organic anion transport. This study was designed to elucidate the link between such transporters and the multicentric occurrence (MO) after radical hepatectomy. Results: SLC22A7 expression was the best predictor of metastasis-free survival (MFS) as judged by the GA (Fold, 0.726; P=0.001). High SLC22A7 gene expression in noncancerous tissue prevent HCC occurrence after hepatectomy (Odds Ratio (OR), 0.2; 95%CI, 0.1-0.6; P=0.004). Multivariate analyses of MFS revealed the independent risk factor to be SLC22A7 expression (OR, 0.3; 95%CI, 0.1-1.0, P=0.043). Low SLC22A7 expression caused MO of HCC significantly (log-rank, P=0.001). In the validation study, multivariate analyses of MFS revealed the independent risk factor to be SLC22A7 expression (OR, 0.5; 95%CI, 0.3-0.8; P=0.012). As judged by Gene set-enrichment analysis, SLC22A7 down-regulation associated with mitochondrion (P=0.008; false discovery rate (FDR)=0.199; normalized enrichment score (NES) =1.804), oxidoreductase activity (P=0.006; FDR=0.157; NES=1.854) and fatty acid metabolic process (P=0.021; FDR=0.177; NES=1.723). Sirtuin3 also determined MFS (P= 0.018). Conclusions: These pathways involving SLC22A7 dysfunction may promote the occurrence of HCC.
2013-04-01 | GSE40873 | GEO
Project description:Background & Aims: The recurrence determines the postoperative prognosis of patients with hepatocellular carcinoma (HCC). It is unknown whether de novo HCCs derive from the liver with disability of an organic anion transport. This study was designed to elucidate the link between such transporters and the multicentric occurrence (MO) after radical hepatectomy. Results: SLC22A7 expression was the best predictor of metastasis-free survival (MFS) as judged by the GA (Fold, 0.726; P=0.001). High SLC22A7 gene expression in noncancerous tissue prevent HCC occurrence after hepatectomy (Odds Ratio (OR), 0.2; 95%CI, 0.1-0.6; P=0.004). Multivariate analyses of MFS revealed the independent risk factor to be SLC22A7 expression (OR, 0.3; 95%CI, 0.1-1.0, P=0.043). Low SLC22A7 expression caused MO of HCC significantly (log-rank, P=0.001). In the validation study, multivariate analyses of MFS revealed the independent risk factor to be SLC22A7 expression (OR, 0.5; 95%CI, 0.3-0.8; P=0.012). As judged by Gene set-enrichment analysis, SLC22A7 down-regulation associated with mitochondrion (P=0.008; false discovery rate (FDR)=0.199; normalized enrichment score (NES) =1.804), oxidoreductase activity (P=0.006; FDR=0.157; NES=1.854) and fatty acid metabolic process (P=0.021; FDR=0.177; NES=1.723). Sirtuin3 also determined MFS (P= 0.018). Conclusions: These pathways involving SLC22A7 dysfunction may promote the occurrence of HCC. The 49 noncancerous liver tissues of HCC patients within Milan criteria, treated at our institution between January 2004 and August 2008, were examined as a training set by genome-wide gene expression analysis (GA). Cox proportional hazards regression analyses for MO-free survival (MFS) were performed to estimate the risk factors. Using the independent two institutional cohorts of 134 patients between September 2008 and December 2009, a validation study was employed using tissue microarrays.
2013-04-01 | E-GEOD-40873 | biostudies-arrayexpress
Project description:Hepatocellular carcinoma (HCC) affects millions of people worldwide and is a lethal malignancy for which there are no effective therapies. To identify prognostic gene markers for liver cancer, we conducted transcriptome profiling of frozen tissues (tumor and non-tumor) from 300 early-to-advanced stage HCCs plus 40 cirrhotic and 6 normal livers. We have profiles 268 HCC tumor, 243 adjacent non-tumor, 40 cirrhotic and 6 healthy liver samples.
2011-07-05 | E-GEOD-25097 | biostudies-arrayexpress
Project description: Not available
| S-EPMC64988 | biostudies-literature
Project description:Chronic infections by hepatitis B virus (HBV) and hepatitis C virus (HCV) appear to be the most significant causes of hepatocellular carcinoma (HCC). Aberrant promoter methylation is known to be deeply involved in cancer, including HCC. In this study, we analyzed aberrant promoter methylation on genome-wide scale in 6 HCCs including 3 HBV-related and 3 HCV-related HCCs, 6 matched noncancerous liver tissues and 3 normal liver tissues by methylated DNA immunoprecipitation-on-chip analysis. Candidate genes with promoter methylation were detected more frequently in HCV-related HCC. Candidate genes methylated preferentially to HBV-related or HCV-related HCCs were detected and selected, and methylation levels of the selected genes were validated using 125 liver tissue samples, including 61 HCCs (28 HBV-related HCCs and 33 HCV-related HCCs) and matched 59 matched noncancerous livers, and 5 normal livers, by quantitative methylation analysis using MALDI-TOF mass spectrometry. Among analyzed genes, preferential methylation in HBV-related HCC was validated in 1 gene only. However, 15 genes were found methylated preferentially in HCV-related HCC, which was independent from age. Hierarchical clustering of HCC using these 15 genes stratified HCV-related HCC as a cluster of frequently methylated samples. The 15 genes included genes inhibitory to cancer-related signaling such as RAS/RAF/ERK and Wnt/b-catenin pathways. It was indicated that genes methylated preferentially in HCV-related HCC exist, and it was suggested that DNA methylation might play an important role in HCV-related HCC by silencing cancer-related pathway inhibitors. we analyzed aberrant promoter methylation in 6 HCC clinical samples (including 3 HBV-related HCCs and 3 HCV-related HCCs) and their matched noncancerous tissues on genome-wide scale by the method. Candidate regions of promoter methylation preferentially to HBV-related HCC and HCV-related HCC were selected, and the methylation levels of these genes were measured quantitatively using MALDI-TOF mass spectrometry. Expression levels of these 6 pairs of HCC and 4 more pairs of HCCs and surrounding noncancerous tissues were analyzed by expression array and are reported in this Series. <br><br>This experiment was reloaded in November 2010 after additional curation. this dataset is part of the TransQST collection.
2010-07-06 | E-GEOD-19665 | biostudies-arrayexpress
Project description:LncRNA profiling of hepatocellular carcinoma vs. matched noncancerous liver tissue, aimed to analyze the lncRNA expression profile of hepatocellular carcinoma (HCC) and identify prognosis-related lncRNAs.
2023-06-25 | GSE72170 | GEO
Project description:To compare the characteristics and mechanisms of Myc and xmrk induced zebrafish liver tumor, next generation sequencing-based SAGE analyses were used to examine the transcriptomes of tumor and control samples. The results indicated that relatively small overlaps of significantly deregulated genes and biological pathways among different zebrafish liver tumor models.Nevertheless, they all significantly correlate with advanced or very advanced human hepatocellular carcinoma (HCC). Molecular signature from each oncogene-induced zebrafish liver tumor correlated with only a small subset of human HCC samples, and they share conserved up-regulated pathways. A short list of commonly deregulated genes among different zebrafish liver tumors showed accordant deregulation in the majority of human HCCs, suggesting that they may serve as common diagnosis markers and therapeutic targets.Thus, these transgenic zebrafish models with well-defined oncogene-induced tumors are valuable tools for molecular classification of human HCCs and for understanding of molecular drivers in hepatocarcinogenesis in each human HCC subgroup. Transcriptome profiling of Myc tumor sample (X-M+D+) and control samples (X-M-D-, X-M+D-, X-M-D+), xmrk tumor sample (X+M-D+) and control samples (X-M-D-, X+M-D-, X-M-D+), were generated by deep sequencing, using 3' RNA-SAGE on SOLiD system
2013-12-17 | E-GEOD-53342 | biostudies-arrayexpress
Project description:To compare the characteristics and mechanisms of Myc and xmrk induced zebrafish liver tumor, next generation sequencing-based SAGE analyses were used to examine the transcriptomes of tumor and control samples. The results indicated that relatively small overlaps of significantly deregulated genes and biological pathways among different zebrafish liver tumor models.Nevertheless, they all significantly correlate with advanced or very advanced human hepatocellular carcinoma (HCC). Molecular signature from each oncogene-induced zebrafish liver tumor correlated with only a small subset of human HCC samples, and they share conserved up-regulated pathways. A short list of commonly deregulated genes among different zebrafish liver tumors showed accordant deregulation in the majority of human HCCs, suggesting that they may serve as common diagnosis markers and therapeutic targets.Thus, these transgenic zebrafish models with well-defined oncogene-induced tumors are valuable tools for molecular classification of human HCCs and for understanding of molecular drivers in hepatocarcinogenesis in each human HCC subgroup.
2013-12-17 | GSE53342 | GEO