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Association of A(313)G glutathione S-transferase P1 germline polymorphism with susceptibility to de novo myelodysplastic syndrome.

Authors: Zachaki, S  Stavropoulou, C  Kalomoiraki, M  Koromila, T  Daraki, A  Manola, KN  Mavrou, A  Kanavakis, E  Pantelias, GE  Sambani, C 
Citation: Zachaki S, etal., Leuk Lymphoma. 2013 Aug;54(8):1756-61. doi: 10.3109/10428194.2012.762647. Epub 2013 Jan 28.
Pubmed: (View Article at PubMed) PMID:23278642
DOI: Full-text: DOI:10.3109/10428194.2012.762647

Models for the pathogenesis of myelodysplastic syndrome (MDS) imply the role of individual genetic variations in genes involved in detoxification mechanisms. GSTP1 enzyme plays a key role in the biotransformation of a variety of carcinogens. The corresponding gene is subject to a single nucleotide polymorphism (A(313)G) leading to abolished enzyme activity. In order to evaluate whether the GSTP1 polymorphism influences MDS susceptibility, we conducted a case-control study comprising 310 de novo patients and 370 healthy controls using a real-time polymerase chain reaction (PCR) genotyping method. The GSTP1 gene status was also evaluated in relation to patients' characteristics and chromosomal abnormalities. A significantly higher incidence of the GSTP1 variant genotypes was observed in patients with MDS compared to controls (p < 0.0001). The results revealed increased frequencies of heterozygotes in patients younger than 60 years old and of homozygotes G/G in older patients (p = 0.007). Our results provide evidence for a pathogenetic role of the GSTP1 polymorphism in MDS risk, probably in an age-dependent manner.


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CRRD Object Information
CRRD ID: 10755416
Created: 2016-01-27
Species: All species
Last Modified: 2016-01-27
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.