BACKGROUND: We examined the level of fragile histidine triad (FHIT) and p16 gene methylation in patients with hepatocellular carcinoma and explored the relationship to liver cancer.

MATERIAL AND METHODS: There were 56 patients with primary liver cancer who were admitted to the hospital from July 2015 to October 2017 included in the liver cancer group, and 24 non-hepatoma patients (hepatitis A/hepatitis B/hepatitis C, liver cirrhosis, liver fibrosis, and fatty liver, alcoholic liver identified as a control group. Fasting venous blood samples were collected from the 2 groups. Methylation-specific PCR (MSP) was used to detect the methylation of FHIT and p16 genes in the 2 groups. The risk factors for lung cancer were analyzed by logistic regression. In addition, the effects of FHIT and p16 gene methylation on the diagnostic accuracy of liver cancer were calculated.

RESULTS: The incidence of FHIT and p16 methylation in serum from the liver cancer group was 51.8% and 67.9%, respectively. The incidence of FHIT and p16 methylation in the non-hepatoma group was 16.7% and 25.0%. There was a statistical statistically correlated with gender, and the methylation of FHIT and p16 genes (P<0.05). From logistic regression analysis results, methylation of p16 and FHIT genes was an independent risk factor for hepatocellular carcinoma with odds ratio (OR) values of 10.550 (2.313~48.116) and 8.239 (2.386~28.455), respectively.

CONCLUSIONS: The methylation of p16 and FHIT genes was an independent risk factor for hepatocellular carcinoma.

Keywords: Liver Neoplasms, Methylation, Vitamin D-Binding Protein, Acid Anhydride Hydrolases, Biomarkers, Tumor, Carcinoma, Hepatocellular, Case-Control Studies, Cyclin-Dependent Kinase Inhibitor p16, DNA Methylation, Genes, p16, Neoplasm Proteins, Promoter Regions, Genetic, Risk Factors