Abstract
Hepatocellular carcinoma (HCC) is one of the most common cancers with a dismal outcome. The complicated molecular pathogenesis of HCC caused by tumor heterogeneity makes it difficult to identify druggable targets useful for treating HCC patients. One approach that has a potential for the improvement of patient prognosis is the identification of cancer driver genes that play a critical role in the development of HCC. Recent technological advances of high-throughput methods, such as gene expression profiles, DNA copy number alterations and somatic mutations, have expanded our understanding of the comprehensive genetic profiles of HCC. Integrative analysis of these omics profiles enables us to classify the molecular subgroups of HCC patients. As each subgroup classified according to genetic profiles has different clinical features, such as recurrence rate and prognosis, the tumor subclassification tools are useful in clinical practice. Furthermore, a global genetic analysis, including genome-wide RNAi functional screening, makes it possible to identify cancer vulnerable genes. Identification of common cancer driver genes in HCC leads to the development of an effective molecular target therapy.
Highlights
Hepatocellular carcinoma (HCC) is one of the most common cancers with a dismal outcome
This review summarizes the current knowledge of tumor heterogeneity and cancer driver genes, in hepatocellular carcinoma (HCC)
The development of HCC is closely associated with multiple risk factors, such as chronic infection of hepatitis B virus (HBV) [17,18] and hepatitis C virus (HCV) [19,20], alcohol consumption [21,22,23], aflatoxin B1 exposure [24,25,26,27,28] and obesity [29]
Summary
Many studies over the past century have revealed that cancer is a genetic disease. Most cancers are thought to develop through the acquisition of genetic alterations and the selection of neoplastic clones in a preferred tumor microenvironment [1,2,3]. The development of HCC is closely associated with multiple risk factors, such as chronic infection of hepatitis B virus (HBV) [17,18] and hepatitis C virus (HCV) [19,20], alcohol consumption [21,22,23], aflatoxin B1 exposure [24,25,26,27,28] and obesity [29] In addition to these common etiological factors, other factors are known to contribute to hepatocarcinogenesis with a low frequency, including non-alcoholic fatty liver disorders, diabetes, hemochromatosis and long-term oral contraceptive use [30,31,32,33,34].
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