216 MIR-100 IS DOWNREGULATED FROM EARLY STAGES OF HEPATOCARCINOGENESIS AND CORRELATES WITH OVEREXPRESSION OF ITS TARGET PLK1

available kits. DNA samples were typed for SNPs: −1195 G>A of COX-2, −308 G>A of TNF-a, +936 C>T of VEGF-A and −174 G>C of IL-6 genes. RFLP-PCR method was used to type the SNPs. sIL-6 were dosed with a commercially available ELISA kit. Results: Our data show a statistically significant difference only for the SNP of VEGF-A +936 C>T between HCC and LC patients (P = 0.039). sIL-6 were higher in G/G compared to C/C genotypes in HCC (z = 2; P = 0.04) and G/G vs G/C (z = 1.8; P < 0.03). sIL-6 in G carriers (G/G+G/C) were higher in HCC 4.8 (0.2–17.5) vs LC patients 2.2 (0.07–11.5) (z = 2.8; P = 0.004). sIL-6 in HCC correlated with G carriers (G/G+G/C) (r = 0.25, P = 0.05). A positive correlation was found between sIL-6 levels and some liver function tests both in LC and in HCC. Conclusions: Our results show that C allele carriers in VEGF-A gene are more frequent in HCC vs LC, and confirm the association between the G carriers in IL-6 gene and higher sIL-6, suggesting that these genetic factors could contribute to the development of HCC.