Progreseffects of stromal cell-derived factor-1 and survivin gene polymorphisms on gastric cancer risk

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Abstract

Stromal-cell derived factor-1 (SDF-1), a CXC chemokine, is important for growth, angiogenesis and metastasis of tumor cells. The SDF1-3'A polymorphism has been investigated in various types of cancer; however, no information is currently available on its role in gastric cancer. Survivin is a member of the inhibitor of apoptosis family of proteins and has a genetic polymorphism (-31G/C) located in the CDE/CHR repressor element of its promoter. In this study, 88 gastric cancer patients and 480 normal healthy control subjects were investigated for the genotype and allelic SDF1-3'A and survivin-31G/C frequencies using polymerase chain reaction-restriction fragment length polymorphism. The SDF1-3'A genotype frequencies for GG, GA and AA were 44.32, 48.86 and 6.92% in patients and 42.71, 47.71 and 9.58% in healthy subjects, respectively. GA+AA genotype frequency and A allele distribution were not identified as significantly different between gastric cancer cases and controls. The survivin frequencies for GG, GC and CC were 20.45, 50 and 29.54% in patients and 33.96, 45 and 21.04% in healthy subjects, respectively. The C carriers (GC+CC genotype) and the C allele were over-represented among the gastric cancer cases (P=0.013 and P=0.0083, respectively). Overall, no statistically significant association was identified for SDF-1 and survivin gene examined alleles and genotypes and any parameter investigated, (e.g., stage, differentiation status and survival). The survivin promoter-31G/C polymorphism may confer an increased susceptibility to gastric cancer, while the SDF1-3'A polymorphism may not be a candidate genetic variant to select individuals at higher risk of developing gastric cancer.

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Liarmakopoulos, E., Theodoropoulos, G., Vaiopoulou, A., Rizos, S., Aravantinos, G., Kouraklis, G., … Gazouli, M. (2013). Progreseffects of stromal cell-derived factor-1 and survivin gene polymorphisms on gastric cancer risk. Molecular Medicine Reports, 7(3), 887–892. https://doi.org/10.3892/mmr.2012.1247

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