Abstract
Diverse modes of genomic alterations in hepatocellular carcinoma
Highlights
Hepatocellular carcinoma (HCC) is a heterogeneous disease with high mortality rate
We have previously shown that hepatitis B virus (HBV) DNA frequently integrates into the human genome, causing diverse changes such as DNA copy number variation, chimeric viral-human transcript fusions, and transcriptional activation [3]
Aside from individual genes mutated in HCC, we examine the diverse modes of genomic alteration in this heterogeneous disease, delineating both conventional mutations and virus-associated changes that contribute to liver oncogenesis
Summary
Hepatocellular carcinoma (HCC) is a heterogeneous disease with high mortality rate. Recent genomic studies have identified TP53, AXIN1, and CTNNB1 as the most frequently mutated genes. Hepatitis B virus (HBV) integrations into the human genome have been associated with HCC. Hepatocellular carcinoma (HCC) is the third leading cause of cancer-related death, with a poor 5-year survival rate of less than 10% [1]. Several emerging themes were revealed by recent genomic studies [3,4,5,6], including recurrent mutations in TP53, Wnt-signaling components CTNNB1 and AXIN1, and structural variations, and virus-mediated mutations. We have previously shown that HBV DNA frequently integrates into the human genome, causing diverse changes such as DNA copy number variation, chimeric viral-human transcript fusions, and transcriptional activation [3]. Given the disruptive nature of HBV integration, it is pertinent to study all modes of genomic changes in the same context
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