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Research Article

The Molecular Diagnosis of Hepatitis B Virus-Associated Hepatocellular Carcinoma

, , &
Pages 69-101 | Published online: 10 Oct 2008
 

Abstract

Hepatitis B virus (HBV) infection is the major cause of hepatocellular carcinoma (HCC) worldwide. The pathogenesis of HBV-associated HCC has been studied extensively, and molecular changes during malignant transformation have been identified. It has been proposed that the insertion of HBV DNA into the human genome results in chromosomal instability and inactivation of tumor suppressor genes. Transactivation of oncogenes, inactivation of tumor suppressor genes, and alteration of the cell cycle by HBV proteins are also involved in the progression of hepatocellular carcinogenesis. Traditional clinical examinations of HCC, such as biopsy, computer tomography, ultrasonic imaging, and detection of such biomarkers as α-fetoprotein, are currently the “gold standard” in diagnosis.These tests diagnose HCC only in the late stages of disease. This limitation has greatly reduced the chance of survival of HCC patients. To resolve this problem, new biomarkers that can diagnose HCC in earlier stages are necessary. Based on recent molecular studies of the effects of HBV on cellular transformation, differentially expressed biomarkers of HBV infection have been elucidated. With the analyses of the HBV replication profile, the viral load (HBV DNA levels) of patients, and the viral protein expression, the severity of hepatitis in the preneoplastic stages can be assessed. In the future, with the molecular profiles identified by genomic and proteomic approaches, stage-specific biomarkers should be identified to monitor the progression and prognosis of HCC.

Abbreviations
AFP,=

α-fetoprotein;

AFP-L3,=

L. culinaris agglutinin-reactive AFP;

AP-1, AP-2,=

transcription factors;

CAH,=

chronic active hepatitis;

cccDNA,=

covalent closed circular DNA;

CT,=

computer tomography;

GGT,=

γ-glutamyltransferase;

H&E,=

hematoxylin and eosin;

HA,=

hyaluronic acid;

HBcAg,=

hepatitis B core antigen;

HBeAg,=

hepatitis B e antigen;

HBsAg,=

hepatitis B surface antigen;

HBSP,=

hepatitis B virus splice-generated protein;

HBV,=

hepatitis B virus;

HBx,=

hepatitis Bx protein;

HCC,=

hepatocellullar carcinoma;

HSP,=

heat shock protein;

hTERT,=

human telomerase reverse transcriptase;

IFN-α,=

interferon α;

IL,=

interleukin;

LC,=

liver cirrhosis;

LGE,=

log genome equivalents;

msAFP,=

monosialylated AFP;

NF-κB,=

transcription factor;

ORF,=

open reading frame;

pCEA,=

polyclonal carcinoembryonic antigen;

PIVKA-II,=

protein induced by vitamin K absence or antagonist-II;

PKC,=

protein kinase C;

RB1,=

retinoblastoma gene;

SOD,=

superoxide dismutase;

TNF,=

tumor necrosis factor;

WHV,=

woodchuck hepatitis virus.

Abbreviations
AFP,=

α-fetoprotein;

AFP-L3,=

L. culinaris agglutinin-reactive AFP;

AP-1, AP-2,=

transcription factors;

CAH,=

chronic active hepatitis;

cccDNA,=

covalent closed circular DNA;

CT,=

computer tomography;

GGT,=

γ-glutamyltransferase;

H&E,=

hematoxylin and eosin;

HA,=

hyaluronic acid;

HBcAg,=

hepatitis B core antigen;

HBeAg,=

hepatitis B e antigen;

HBsAg,=

hepatitis B surface antigen;

HBSP,=

hepatitis B virus splice-generated protein;

HBV,=

hepatitis B virus;

HBx,=

hepatitis Bx protein;

HCC,=

hepatocellullar carcinoma;

HSP,=

heat shock protein;

hTERT,=

human telomerase reverse transcriptase;

IFN-α,=

interferon α;

IL,=

interleukin;

LC,=

liver cirrhosis;

LGE,=

log genome equivalents;

msAFP,=

monosialylated AFP;

NF-κB,=

transcription factor;

ORF,=

open reading frame;

pCEA,=

polyclonal carcinoembryonic antigen;

PIVKA-II,=

protein induced by vitamin K absence or antagonist-II;

PKC,=

protein kinase C;

RB1,=

retinoblastoma gene;

SOD,=

superoxide dismutase;

TNF,=

tumor necrosis factor;

WHV,=

woodchuck hepatitis virus.

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