Author(s): Borges Bdo N, Burbano RR, Harada ML
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Abstract Gastric cancer, despite its decline in incidence, remains a public health problem worldwide, especially in Brazil, where higher incidence indexes are still described. The Survivin gene codifies a multifunctional protein involved in the regulation of the cell cycle and inhibition of the apoptotic pathway, and a polymorphism (-31C/G) located in its promoter region is associated with gene regulation. In order to evaluate the correlation of this polymorphism with gastric cancer risk in a northern Brazil population, we sequenced a fragment containing the polymorphism in individuals with gastric cancer and controls. We observed no differences of alleles and genotype frequencies between cases and controls. However, G carriers of the tumor group had an increased relative risk of developing tumors of diffuse type (OR: 2.22-IC 95\%: 0.4835-10.2137), localized in the antrum (OR: 2.16-IC 95\%: 0.4811-9.6971) and in younger patients (<50 years-old) (OR: 3.65-IC 95\%: 0.4012-33.2429), although with no statistical significance. Nevertheless, C carriers with a high D17S250 microsatellite instability (TP53 gene) show a higher risk to develop gastric tumors (P = 0.0453; OR: 4.1556-IC95\%: 0.9716-17.7728), suggesting that the mutate TP53 gene may fail in control and inhibition of Survivin expression, favoring the gastric carcinogenesis. The present result suggests that the presence of the C allele of -31C/G Survivin promoter polymorphism in combination with D17S250 instability may be used as a risk factor for gastric cancer in our population. However, other studies based on a larger sample size are required to properly assess such hypothesis.
This article was published in Clin Exp Med
and referenced in Journal of Cancer Science & Therapy