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Survivin gene promoter polymorphism ‐31G/C as a risk factor for keratocystic odontogenic tumor development
Author(s) -
Andric Miroslav,
Nikolic Nađa,
Boskovic Marija,
Milicic Biljana,
Skodric Sanja,
Basta Jovanovic Gordana,
Milasin Jelena
Publication year - 2012
Publication title -
european journal of oral sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.802
H-Index - 93
eISSN - 1600-0722
pISSN - 0909-8836
DOI - 10.1111/j.1600-0722.2011.00919.x
Subject(s) - genotype , biology , survivin , single nucleotide polymorphism , allele , keratocystic odontogenic tumor , genetics , promoter , gastroenterology , gene , microbiology and biotechnology , medicine , oncology , pathology , odontogenic , gene expression
Andric M, Nikolic N, Boskovic M, Milicic B, Skodric S, Basta Jovanovic G, Milasin J. Survivin gene promoter polymorphism ‐ 31G/C as a risk factor for keratocystic odontogenic tumor development.
Eur J Oral Sci 2012; 120: 9–13. © 2012 Eur J Oral Sci Several single nucleotide polymorphisms in survivin gene promoters, notably ‐31G/C, have been shown to modulate the expression and activity of the survivin protein. Consequently, the ‐31G/C polymorphism has been identified as a risk factor for the development of several types of tumors. The aim of this study was to investigate a possible association between the ‐31G/C polymorphism and the risk for keratocystic odontogenic tumor (KCOT) development. DNA from 52 biopsy specimens of KCOTs and from 82 buccal swabs of healthy individuals was subjected to PCR restriction fragment length polymorphism analysis to identify individual genotypes. The distribution of genotypes in KCOT and control groups, respectively, was: GG: 30 (57.7%) vs. 26 (31.7%); CG: 17 (32.7%) vs. 45 (54.9%); and CC: 5 (9.6%) vs. 11 (13.4%), respectively. These differences were statistically significant. The G allele was more common in the KCOT group than in the control group: 76 (74%) vs. 96 (59%), respectively. Logistic regression analysis showed that GC heterozygotes had a considerably decreased susceptibility for KCOTs compared with GG homozygotes. The same was true for GC+CC vs. GG. The GG genotype of the ‐31G/C polymorphism might be a risk factor for KCOT development.