[The relationship between the KIF1B (rs17401966) single nucleotide polymorphism and the genetic susceptibility to Hepatocellular carcinoma].

OBJECTIVE: To study the relationship between SNP rs17401966 at the KIF1B gene and the genetic susceptibility to Hepatocellular carcinoma (HCC). METHODS: All study objects were recruited from two Grade A hospitals of Amoy from January 2011 to October 2014.They were surveyed in individual matching case-control study. Accepting criterias in the cases: HCC was first diagnosed based on diagnostic basis during the investigations, over 18 years old, present addresses were as same as surveyed areas in the district (county) level range, no past history of cancers; Exclusion criterias: patients with other liver diseases. The tumor patients without HCC, patients with autoimmune hepatitis or toxic hepatitis, patients who refused to be investigated or too ill to be investigated. Accepting criterias in the controls: the control who passed the physical examination matched the case in ages (no more than 3 years old), sex, health screening in the same hospital over the same period and district (county); Exclusion criterias: people with liver disease or any history of cancers. This study consisted of 376 HCC patients and 403 controls, 5 ml morning fasting venous blood of all subjects were obtained to isolate cells and distribute genotype. The differences in general information between cases and controls were tested by χ² test and t-test. The association between SNP rs17401966 and the risk of developing HCC were assessed by using the multiple factors logistic regression. RESULTS: The mean age and standard deviation for case and control groups were (61.7 ± 12.8) years and (60.6 ± 12.7) years (t = 1.15, P = 0.251), respectively. The proportion of family history of cancer [28.7% (108/376)] and the HBsAg positive rate [26.9 % (101/376)] in case group were higher than these in control group [15.9% (64/403), 2.7% (11/403)] (χ² = 18.65, 92.02, P < 0.001). In HBsAg carriers, GG genotype genetic susceptibility to HCC is 0.12 (0.02-0.75) times for AA genotype, and G allele susceptibility to HCC is 0.38 (0.15-0.98) times for A allelc. In HBsAg negative group, it showed no statistical significance in the relationship between SNP rs17401966 and susceptibility to HCC, and compared with the A allele, the risk for HCC of G allele is 0.79 (0.62-1.01). CONCLUSION: The results demonstrated that the presence of the GG genotype, the GA genotype and the G allele at rs17401966 of the KIF1B gene might decrease the risk for HCC.