title: Hepatitis B viral load affects prognosis of hepatocellular carcinoma.
abstract: Hepatocellular carcinoma (HCC) is a complex disease that is dually challenging to treat due to underlying chronic liver disease in addition to the cancer itself. The prognosis of patients with HCC is determined by intrahepatic tumor status and reserved hepatic function. Hepatitis B virus (HBV) is an established major risk factor of HCC development, and HBV viral load is being increasingly recognized as a prognostic factor in the presence of established HCC. High HBV viral load may affect the prognosis of HBV-related HCC patients in several ways. First, it is associated with more frequent recurrence of HBV-related HCC after treatment. Second, it is associated with more occurrence and severity of potentially life-threatening HBV reactivation. Last, it is associated with more worsened liver function, which limits the therapeutic options for HBV-related HCC. HBV, directly or indirectly, can induce hepatocarcinogenesis. In patients with a high HBV DNA level and subsequent active hepatitis, adhesion molecules expressed on the sinusoidal cells are up-regulated and may increase intrahepatic metastasis. HCC progression after treatment can lead to a poor prognosis by reducing number of normal functioning hepatocytes. Thus, high HBV viral load can affect the prognosis of patients with HCC by frequent recurrence after treatment for HCC and deterioration of hepatic function associated with HCC progression. Recent meta-analysis showed that antiviral treatment reduces HCC recurrence and liver-related mortality after curative therapy of HCC. Given the strong relationship between high HBV DNA load and poor survival outcome of HCC patients due to cancer progression, it is expected that long-term antiviral therapy results in the sustained HBV suppression, control of inflammation, reduction in HCC progression, and eventually in improved overall survival.
authors.affiliation: Su Jong Yu, Yoon Jun Kim, Department of Internal Medicine and Liver Research Institute, Seoul National University College of Medicine, Seoul 110-744, South Korea.
authors.forename: Su Jong
authors.initials: SJ
authors.lastname: Yu
authors.affiliation: Su Jong Yu, Yoon Jun Kim, Department of Internal Medicine and Liver Research Institute, Seoul National University College of Medicine, Seoul 110-744, South Korea.
authors.forename: Yoon Jun
authors.initials: YJ
authors.lastname: Kim
mesh_terms: D000818:Animals; D000998:Antiviral Agents / Q000627:therapeutic use; D015415:Biomarkers / Q000097:blood; D006528:Carcinoma, Hepatocellular / Q000401:mortality / Q000473:pathology / Q000628:therapy / Q000821:virology*; D004279:DNA, Viral / Q000097:blood; D006509:Hepatitis B / Q000150:complications / Q000175:diagnosis / Q000188:drug therapy / Q000401:mortality / Q000821:virology*; D006515:Hepatitis B virus / Q000187:drug effects / Q000235:genetics / Q000472:pathogenicity*; D054884:Host-Pathogen Interactions; D006801:Humans; D008113:Liver Neoplasms / Q000401:mortality / Q000473:pathology / Q000628:therapy / Q000821:virology*; D009364:Neoplasm Recurrence, Local; D012008:Recurrence; D012307:Risk Factors; D013997:Time Factors; D016896:Treatment Outcome; D019562:Viral Load; D014775:Virus Activation
chemical_list: D000998:Antiviral Agents; D015415:Biomarkers; D004279:DNA, Viral
keywords: DNA; Hepatitis B virus; Hepatocellular carcinoma; Prognosis; Progression