Abstract
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 (A313G) 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.
Acknowledgements
The authors wish to thank Prof. P. Kollia for her valuable suggestions. We acknowledge E. M. Delicha for statistical analysis; and K. Stavropoulou and V. Diamantopoulou for excellent technical assistance.
Potential conflict of interest:
Disclosure forms provided by the authors are available with the full text of this article at www.informahealthcare.com/lal.
This work has been co-financed by the European Union (European Social Fund, ESF) and Greek National funds through the Operational Program “Education and Lifelong Learning” of the NSRF-Research Funding Program “Heracleitus II.”