Hepatitis B virus (HBV) infection plays a major role in hepatocellular carcinoma (HCC) development. Much evidence suggests that HBV also maintains its pro-oncogenic properties in cases of occult HBV infection (OBI). Mutations of the beta-catenin and p53 genes (CTNNB1 and TP53, respectively) may be associated with HCC occurrence in patients with overt HBV infection, whereas such genetic mutations have not been investigated in HCC patients with OBI thus far. We investigated the genetic heterogeneity of CTNNB1 exon 3 and all of the TP53 exons in tumor DNA extracts from a unique cohort of 61 HCC patients (all previously tested for HBV DNA and for its integration into the host's genome), including 34 OBI-positive, 20 HBV surface antigen (HBsAg)/OBI-negative, and 7 HBsAg-positive cases. No CTNNB1 exon 3 mutations or TP53 mutations were detected in any case. The homo- or heterozygous TP53 R72P polymorphism was found in 18 of 61 cases (29.5%), although no differences in its prevalence between OBI and non-OBI cases as well as between cases with and without viral integration were revealed. In conclusion, CTNNB1 and TP53 somatic mutations seem to be a rare event in patients with HCC in our area and in cases with either overt or occult HBV infection.
Keywords: CTNNB1; Hepatocellular carcinoma; Occult hepatitis B; TP53.
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