Hepatitis B 1762T/1764A mutations, hepatitis C infection, and codon 249 p53 mutations in hepatocellular carcinomas from Thailand

Shuang Yuan Kuang, Suree Lekawanvijit, Niwat Maneekarn, Satawat Thongsawat, Kimberly Brodovicz, Kenrad Edwin Nelson, John Davis Groopman

Research output: Contribution to journalArticle

Abstract

Hepatocellular carcinoma is one of the leading causes of cancer death worldwide. The etiology of liver cancer is multifactorial, and infection with hepatitis B virus (HBV), whose pathogenesis is exacerbated by the acquisition of mutations that accelerate carcinogenesis, or hepatitis C virus (HCV) and dietary exposure to aflatoxin B1 all contribute to elevating one's risk for this disease. In this study, we sought to determine the contributions of these agents by measuring the occurrence of an HBV 1762T/1764 A double mutation, an aflatoxin-specific 249G→T mutation of the p53 gene, and HCV in plasma of 34 HCC cases and 68 age- and gender-matched controls, and in 25 liver tumors from northern Thailand. In total, 14 cases, 5 controls, and 19 tumors had detectable levels of HBV DNA. All 14 cases, 2 controls (2.9%), and 17 tumors (89.5%) were positive for the HBV double mutation. Nine cases (26.5%), 10 controls (14.7%), and 6 tumors (24%) were positive for the p53 mutation. Five cases (14.7%), no controls, and 4 rumors (16%) had both mutations. The median age of HCC diagnosis in these 5 cases was 34 years versus 51 years for other cases. Five cases (14.7%) and 1 control (1.5%) were HCV enzyme immunoassay positive. Thus, specific HBV, HCV, and aflatoxin biomarkers reveal the complexity of risks contributing to HCC in northern Thailand and suggest further application of these biomarkers as intermediate end points in prevention, intervention trials, and etiologic investigations.

Original languageEnglish (US)
Pages (from-to)380-384
Number of pages5
JournalCancer Epidemiology Biomarkers and Prevention
Volume14
Issue number2
DOIs
StatePublished - Feb 2005

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Thailand
Hepatitis C
Hepatitis B
Codon
Hepatocellular Carcinoma
Hepatitis B virus
Hepacivirus
Mutation
Infection
Aflatoxins
Neoplasms
Biomarkers
Aflatoxin B1
p53 Genes
Liver Neoplasms
Immunoenzyme Techniques
Cause of Death
Carcinogenesis
Liver
DNA

ASJC Scopus subject areas

  • Epidemiology
  • Oncology

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Hepatitis B 1762T/1764A mutations, hepatitis C infection, and codon 249 p53 mutations in hepatocellular carcinomas from Thailand. / Kuang, Shuang Yuan; Lekawanvijit, Suree; Maneekarn, Niwat; Thongsawat, Satawat; Brodovicz, Kimberly; Nelson, Kenrad Edwin; Groopman, John Davis.

In: Cancer Epidemiology Biomarkers and Prevention, Vol. 14, No. 2, 02.2005, p. 380-384.

Research output: Contribution to journalArticle

Kuang, Shuang Yuan ; Lekawanvijit, Suree ; Maneekarn, Niwat ; Thongsawat, Satawat ; Brodovicz, Kimberly ; Nelson, Kenrad Edwin ; Groopman, John Davis. / Hepatitis B 1762T/1764A mutations, hepatitis C infection, and codon 249 p53 mutations in hepatocellular carcinomas from Thailand. In: Cancer Epidemiology Biomarkers and Prevention. 2005 ; Vol. 14, No. 2. pp. 380-384.
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