AIM: To assess the relationship between vitamin D re-ceptor (VDR) gene polymorphisms and the presence of hepatocellular carcinoma (HCC). METHODS: Two-hundred forty patients who underwent liver transplantation were studied. The etiologies of liver disease were hepatitis C (100 patients), hepatitis B (37) and alcoholic liver disease (103). A group of 236 healthy subjects served as controls. HCC in the explanted liver was detected in 80 patients. The following single nucle-otide gene polymorphisms of the VDR were investigatedby polymerase chain reaction and restriction fragment length polymorphism: FokI C>T (F/f), BsmI A>G (B/b), ApaI T>G (A/a) and TaqI T>C (T/t) (BAT). RESULTS: The frequencies of genotypes in patients without and with HCC were for FokI F/F = 69, F/f = 73, f/f = 18 and F/F = 36, F/f = 36, f/f = 8; BsmI b/b = 45, B/b = 87, B/B = 28 and b/b = 33, B/b = 35, B/B = 12; for ApaI A/A = 53, A/a = 85, a/a = 22 and A/A = 27, A/a = 38, a/a = 15; for TaqI T/T = 44, T/t = 88, t/t = 28 and T/T = 32, T/t = 38, t/t = 10. Carriage of the b/b genotype of BsmI and the T/T genotype of TaqI was signif icantly associated with HCC (45/160 vs 33/80, P < 0.05 and 44/160 vs 32/80, P < 0.05, respectively). The absence of the A-T-C protective allele of BAT was signif i-cantly associated with the presence of HCC (46/80 vs 68/160, P < 0.05). A strong association was observed between carriage of the BAT A-T-C and G-T-T haplotypes and HCC only in alcoholic liver disease (7/46 vs 12/36 vs 11/21, P < 0.002, respectively).CONCLUSION: VDR genetic polymorphisms are sig-nificantly associated with the occurrence of HCC in patients with liver cirrhosis. This relationship is more specific for patients with an alcoholic etiology. AIM: To assess the relationship between vitamin D re-ceptor (VDR) gene polymorphisms and the presence of hepatocellular carcinoma (HCC). METHODS: Two-hundred forty patients who underwent liver transplantation were studied. The etiologies of liver disease were hepatitis C 100 patients), hepatitis B (37) and alcoholic liver disease (103). A group of 236 healthy subjects served as controls. HCC in the explanted liver was detected in 80 patients. The following single nucleotide-nucleotide gene polymorphisms of the VDR were PCR by polymerase chain reaction and restriction fragment length polymorphism: FokI C> T (F / f), BsmI A> G (B / b), ApaI T> G (A / a) and TaqI T> C (T / t) BAT). RESULTS: The frequencies of genotypes in patients without and with HCC were for FokI F / F = 69, F / f = 73, f / f = 18 and F / F = 36, F / f = 36, f = 8; BsmI b / b = 45, B / b = 87, B / B = 28 and b / b = 33, B / b = 35, B / B = 12; for ApaI A / A = 53, A / a = 85, a / a = 22 and A / A = 27, A / a = 38, a / a = 15; for TaqI T / T = 44, T / t = 88, t / t = 28 and T / T = 32, T / t = 38, t / t = 10. Carriage of the b / b genotype of BsmI and the T / T genotype of TaqI was signif icantly associated with HCC (45/160 vs 33/80 , P <0.05 and 44/160 vs 32/80, P <0.05, respectively). The absence of the ATC protective allele of BAT was signif i-cantly associated with the presence of HCC (46/80 vs 68/160, P <0.05). A strong association was observed between carriage of the BAT ATC and GTT haplotypes and HCC only in alcoholic liver disease (7/46 vs 12/36 vs 11/21, P <0.002, respectively) .CONCLUSION: VDR genetic polymorphisms are sig-nificantly associated with the occurrence of HCC in patients with liver cirrhosis. This relationship is more specific for patients with an alcoholic etiology.