Project description:We profiled the mutations and gene expressions of early and advanced hepatocellular carcinoma (HCC) related with Hepatitis B-viral infection. Integrative analysis was performed with whole-exome sequencing and gene expression profiles of the 12 cases of early and advanced HCCs and paired non-tumoral adjacent liver tissues.
Project description:We profiled the mutations and gene expressions of early and advanced hepatocellular carcinoma (HCC) related with Hepatitis B-viral infection. Integrative analysis was performed with whole-exome sequencing and gene expression profiles of the 12 cases of early and advanced HCCs and paired non-tumoral adjacent liver tissues. 12 HCC Samples
Project description:UNLABELLED:Genetic alterations in specific driver genes lead to disruption of cellular pathways and are critical events in the instigation and progression of hepatocellular carcinoma (HCC). As a prerequisite for individualized cancer treatment, we sought to characterize the landscape of recurrent somatic mutations in HCC. We performed whole-exome sequencing on 87 HCCs and matched normal adjacent tissues to an average coverage of 59×. The overall mutation rate was roughly two mutations per Mb, with a median of 45 nonsynonymous mutations that altered the amino acid sequence (range, 2-381). We found recurrent mutations in several genes with high transcript levels: TP53 (18%); CTNNB1 (10%); KEAP1 (8%); C16orf62 (8%); MLL4 (7%); and RAC2 (5%). Significantly affected gene families include the nucleotide-binding domain and leucine-rich repeat-containing family, calcium channel subunits, and histone methyltransferases. In particular, the MLL family of methyltransferases for histone H3 lysine 4 were mutated in 20% of tumors. CONCLUSION:The NFE2L2-KEAP1 and MLL pathways are recurrently mutated in multiple cohorts of HCC.
Project description:HLA class I ligandome dataset obtained from hepatocellular carcinoma (HCC) as well as corresponding adjacent benign liver tissue (n=16) characterizing respective HLA immunoprecipitates. Additionally, from a subset of the mentioned HCC/ adjacent benign liver samples datasets gained from shotgun protein identification, comprising HCC as well as adjacent benign liver tissue (n=7) are provided. Further, for one patient shotgun protein identification was also performed in serum (blood) samples obtained after HCC recurrence.
Project description:Six pairs of hepatocellular carcinoma and their corresponding non-tumrous liver parenchymas were analyzed to identify the genes differentially expressed in hepatocellular carcinoma and nontumorous liver parenchyma.
Project description:The aim of this study was to identify chemoresistance-associated genes in hepatocellular carcinoma (HCC). cDNA microarray analysis was performed to compare the mRNA expression profiles of a human metastatic HCC cell line (named MHCC97Low) and its derived chemoresistant sublines including cisplatin resistant subline (named MHCC97L/CisR or C8) and doxorubicin resistant subline (named MHCC97L/DoxR or D5).
Project description:<p>Genetic alterations in specific driver genes lead to disruption of cellular pathways and are critical events in the instigation and progression of hepatocellular carcinoma. As a prerequisite for individualized cancer treatment, we sought to characterize the landscape of recurrent somatic mutations in hepatocellular carcinoma. We performed whole exome sequencing on 87 hepatocellular carcinomas and matched normal adjacent tissues to an average coverage of 59x. The overall mutation rate was roughly 2 mutations per Mb, with a median of 45 non-synonymous mutations that altered the amino acid sequence (range 2 to 381). We found recurrent mutations in several genes with high transcript levels: TP53 (18%), CTNNB1 (10%), KEAP1 (8%), C16orf62 (8%), MLL4 (7%) and RAC2 (5%). Significantly affected gene families include the nucleotide-binding domain and leucine rich repeat containing family, calcium channel subunits, and histone methyltransferases. In particular, the MLL family methyltransferases for histone H3 lysine 4 were mutated in 20% of tumors. Conclusion: The NFE2L2-KEAP1 and MLL pathways are recurrently mutated in multiple cohorts of hepatocellular carcinoma.</p>
Project description:Six pairs of hepatocellular carcinoma and their corresponding non-tumrous liver parenchymas were analyzed to identify the genes differentially expressed in hepatocellular carcinoma and nontumorous liver parenchyma. We analyzed mRNA expression pattern of 6 primary hepatocellular carcinomas and their corresponding nontumourous liver parenchyma. The specimens were obtained from a tissue bank in our hospital. All the clinical informations were de-linked from the specimens.