There is evidence to suggest that polymorphic variations in the glutathione S-transferase (GSTs) are associated with cancer susceptibility. The GST supergene family includes several genes with well characterized polymorphisms. Approximately 50% of the Caucasian population is homozygous for deletions in GSTM1 and approximately 20% are homozygous for deletions in GSTT1. Deletions lead to an absence of the protein, thus resulting in conjugation deficiency of mutagenic electrophiles to glutathione. The GSTP1 gene displays a polymorphism at codon 105 resulting in an Ile to Val substitution, which alters the enzymatic activity of the protein, and this has been suggested as a putative high-risk genotype in various cancers. In the present study, we investigated the relationship between GSTs polymorphism and the susceptibility to neuroblastoma, comparing GSTs genotypes of 256 children with neuroblastoma with those of 392 normal control subjects. No significant differences of allele frequencies were found between patients and controls. Within the neuroblastoma group, we further investigated whether any particular GSTs genotype was correlated with clinical and biological characteristics at diagnosis, but no association was detected. Our data do not support an important effect of GSTs genotype on neuroblastoma susceptibility.
|Number of pages||4|
|Journal||Pharmacogenetics and Genomics|
|Publication status||Published - Jun 2005|
- Genetic polymorphism
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