BioProject

Hepatocellular carcinoma (HCC), one of most common cancers worldwide, causes more than 600,000 deaths annually and is especially prevalent in China. More...

Hepatocellular carcinoma (HCC), one of most common cancers worldwide, causes more than 600,000 deaths annually and is especially prevalent in China. HCC is associated with multiple risk factors, including infection with the hepatitis B virus (HBV) or hepatitis C virus (HCV), alcohol consumption and aflatoxin B1 (AFB1) contamination of food. In China, HBV infection is a major risk factor for HCC. HCC is a highly malignant cancer with a propensity to infiltrate and metastasize to adjacent and other tissues. HCC patients with portal vein tumor thromboses (PVTTs), which is caused by tumor invasion and metastasis via the intrahepatic portal vein, have extremely poor prognoses because PVTT can lead to the widespread dissemination of the tumor throughout the liver. HCC is thought to arise from genetic lesions, usually in the context of hepatic cirrhosis. Previous investigations have implicated the somatic mutation-induced inactivation of tumor suppressor genes (such as TP53) and activation of oncogenes (such as β-catenin and gp130) in the development of HCC. However, the genetic events underlying HCC oncogenesis and progression are poorly understood. Genetic aberrations are known to be necessary for tumorigenesis and metastasis. However, the identification thus far of only a relatively low frequency of somatic mutations in a small number of genes in clinical HCC samples suggests the possibility of the further identification of a large number of genetic mutations responsible for HCC oncogenesis and progression. Most recently, exomic sequencing has also been applied to HCV-associated HCC, with the finding that ARID2 is commonly mutated in this tumor subtype. However, similar exomic sequencing has not yet been performed in HBV-associated HCC. We believe that the present work will significantly further our understanding of HCC pathogenesis and progression. Less...