Molecular signature in three types of hepatocellular carcinoma with different viral origin by oligonucleotide microarray

Gene Expression Analysis in HBV Transgenic Mouse Liver: A Model to Study Early Events Related to Hepatocarcinogenesis

“…Recent studies have identified numerous epigenetic changes, such as promoter CpG island methylation, that are responsible for inactivation of tumor suppressor genes (38)(39)(40)(41). Gene expression profiles of HCCs with different etiology show different molecular signatures (42,43), suggesting that heterogeneous hepatocarcinogenetic pathways, involved in cell proliferation, cell cycle, apoptosis, and angiogenesis, exist and are deregulated in hepatocarcinogenesis.…”

“…In particular, gene expression profile analysis, using DNA microarray technique, has paved a way to better understand molecular mechanisms in the development of HCC (42,43). Among the enormous number of deregulated genes, however, we still need to identify the "critical" genes that play a pivotal role in initiation and/or promotion of the development of HCC and distinguish them from "bystander" genes as a result of epigenetic interaction.…”

Cell cycle regulation and hepatocarcinogenesis

“…Expression profiling of differentially expressed genes in human liver tumor samples using high density CDNA or oligonucleotide arrays has led to the identification of a large series of genes that are differentially regulated in vivo [12][13][14][15][16][17][18][19][20][21][22][23][24][25][26][27][28] and also support the notion of multiple HCC phenotypes as discussed above. However, a major limitation of expression profiling performed thus far is that it provides only a snapshot of a single point in time and therefore could not distinguish those differences in gene expression that are primary effectors of dysregulated growth from those that represent downstream, or secondary consequences.…”

Gene expression profiling in hepatocellular carcinoma: upregulation of genes in amplified chromosome regions

“…The results provided new information on classification, aetiology, survival prediction, and identification of signalling pathways that could serve as therapeutic targets. [1][2][3][4][5] Functional genomics integrating comparison with genetically modified mice as models for human hepatocellular carcinoma 6 as well as data from promoter regions, 7 expression of non-coding genes, that is, microRNA, 8 or array-based comparative genomic hybridisation (aCGH) 9 has further increased the reliability and significance of the biological and clinical conclusions drawn from gene expression profiles. This will be the basis for developing new targeted therapies, an urgent need to reduce the mortality from hepatocellular carcinoma, which represents the fourth most common malignant tumour with more than one million patients affected worldwide per year, and usually has a very poor prognosis.…”