Objective: : Coagulation factor VII (FVII) triggers the extrinsic pathway of blood coagulation. In our previous study, we showed that FVII plays an important role in tumorigenesis of hepatocellular carcinoma (HCC). However, the role of FVII polymorphism in HCC is still unknown. The present study aimed to investigate the relationship between HCC carcinogenesis and single nucleotide polymorphism of FVII.
Methods: : Thirty-seven HCC patients and 30 healthy donors were recruited in this study. Four common FVII gene polymorphisms - a decanucleotide insertion at position -323 (-323ins10-bp), a G to T substitution at position -401 (-401G/T), a G to A substitution at position -402 (-402G/A), and a T to C substitution at position -122 (-122T/C) - were analyzed by sequencing or commercialized assays using genomic DNA isolated from blood samples. Clinicopathological parameters between control and HCC subjects were compared according to the specific genotypes.
Results: : The most common nucleotide variation was -402G/A. However, no statistically significant difference was observed between healthy controls and HCC subjects for all four polymorphisms in terms of genotype distribution and allele frequencies, indicating that these polymorphisms may not affect HCC tumorigenesis. Furthermore, no association was found between -402G/A polymorphisms and tumor stage, recurrence, and overall survival.
Conclusions: : Our results indicate that FVII polymorphisms may not be a key factor that clinically impact tumorigenesis and outcomes of HCC, although further investigations should be conducted to confirm our findings.
Keywords: Factor VII; cancer; gene; hepatocellular; liver; polymorphism; survival.