European journal of gastroenterology & hepatology · 2010
T1653 mutation in the enhancer II region of the hepatitis B virus genome in southern African Blacks with hepatocellular carcinoma.
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Welschinger Robert, Kew Michael C, Viana Raquel, Badri Motasim
Аннотация
BACKGROUND: An increased incidence of C-to-T1653 transversion (T1653) in the enhancer II region of the core promoter of hepatitis B virus has been reported in Japanese and Chinese patients with hepatocellular carcinoma infected with genotypes B or C of the virus, but little information is available in patients infected with other genotypes.
AIM: To document the prevalence of T1653 in Black Africans with hepatocellular carcinoma, in whom genotype A is the dominant genotype and subgenotype A1 the dominant subgenotype, and to correlate its presence with other core promoter mutations previously described in association with T1653.
METHODS: The presence of the mutations was determined in 84 patients with hepatitis B virus-induced hepatocellular carcinoma and 50 matched asymptomatic carriers of the virus by extracting viral DNA from serum, amplification by polymerase chain reaction assay, and nucleotide sequencing.
RESULTS: T1653 was not found significantly more often in the cancer patients with genotype A and subgenotype A1 than in the controls. An association was found not only between T1653 and T1762, A1764 and dual T1762/A1764 in the patients with hepatocellular carcinoma, but also in the asymptomatic carriers.
CONCLUSION: T1653 mutation of hepatitis B virus does not occur more often in Black African patients with hepatocellular carcinoma with genotype A and subgenotype A1 than in asymptomatic carriers of the virus. No correlation specific to hepatocellular carcinoma was found between T1653 and other core promoter mutations in these patients. The presence of the T1653 mutation did not influence the e antigen status of the patients.
AIM: To document the prevalence of T1653 in Black Africans with hepatocellular carcinoma, in whom genotype A is the dominant genotype and subgenotype A1 the dominant subgenotype, and to correlate its presence with other core promoter mutations previously described in association with T1653.
METHODS: The presence of the mutations was determined in 84 patients with hepatitis B virus-induced hepatocellular carcinoma and 50 matched asymptomatic carriers of the virus by extracting viral DNA from serum, amplification by polymerase chain reaction assay, and nucleotide sequencing.
RESULTS: T1653 was not found significantly more often in the cancer patients with genotype A and subgenotype A1 than in the controls. An association was found not only between T1653 and T1762, A1764 and dual T1762/A1764 in the patients with hepatocellular carcinoma, but also in the asymptomatic carriers.
CONCLUSION: T1653 mutation of hepatitis B virus does not occur more often in Black African patients with hepatocellular carcinoma with genotype A and subgenotype A1 than in asymptomatic carriers of the virus. No correlation specific to hepatocellular carcinoma was found between T1653 and other core promoter mutations in these patients. The presence of the T1653 mutation did not influence the e antigen status of the patients.