title: Association between glutathione S-transferase genotypes and Hodgkin's lymphoma risk and prognosis.
abstract: OBJECTIVE
  The interplay between genetic susceptibility and exposure to carcinogens has been shown to be involved in the etiology of many solid tumors. We studied the frequency and clinical correlates of polymorphisms resulting in deletions of two genes involved in the detoxification of potentially carcinogenic agents, glutathione S-transferase (GST)-M1 and GSTT1 in patients with Hodgkin's lymphoma (HL).
  
  
  METHODS
  The prevalence of gene deletions in 90 patients with HL was compared with a case-matched cohort of 176 normal blood donors. GST gene polymorphisms were studied using a multiplex PCR method, including the BCL2 gene as an internal control.
  
  
  RESULTS
  Deletions of the GSTT1 gene were more frequent in cases compared with controls (28.9 versus 17.6%, P = 0.04), resulting in an increased risk for HL in individuals with the GSTT1-null genotype (odds risk, 1.9; 95% confidence interval 1.04-3.46). The GSTT1-null genotype particularly increased the HL risk in females aged <45 years (odds risk 6.1, 95% confidence interval 1.6-23, P = 0.008). Correlating patient characteristics to genotype, we found an association between the GSTT1-null genotype and a limited stage of disease (I/IIA versus IIB-IV, 40.6 versus 19.6%, P = 0.047) and an erythrocyte sedimentation rate of <50 mm/h (P = 0.02). Patients with at least one GST deletion (GSTM1- or GSTT1-) had a significant better disease-free survival when compared with those with undeleted GST genes (GSTM1+/GSTT1+; P = 0.012).
  
  
  CONCLUSIONS
  The GSTT1-null genotype may increase the risk for HL and is associated with favorable prognostic factors, and the presence of at least one GST deletion indicates an improved disease-free survival.
authors.affiliation: Istituto di Ematologia, Universita' Cattolica S Cuore, 00168 Rome, Italy. stefanhohaus@hotmail.com
authors.forename: Stefan
authors.initials: S
authors.lastname: Hohaus
authors.forename: Giuseppina
authors.initials: G
authors.lastname: Massini
authors.forename: Francesco
authors.initials: F
authors.lastname: D'Alo'
authors.forename: Francesco
authors.initials: F
authors.lastname: Guidi
authors.forename: Rossana
authors.initials: R
authors.lastname: Putzulu
authors.forename: Alessandra
authors.initials: A
authors.lastname: Scardocci
authors.forename: Andras
authors.initials: A
authors.lastname: Rabi
authors.forename: Anna Laura
authors.initials: AL
authors.lastname: Di Febo
authors.forename: Maria Teresa
authors.initials: MT
authors.lastname: Voso
authors.forename: Giuseppe
authors.initials: G
authors.lastname: Leone
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D002454:Cell Differentiation; D018572:Disease-Free Survival; D005260:Female; D017353:Gene Deletion; D019254:Genes, bcl-2 / Q000235:genetics; D005838:Genotype; D005982:Glutathione Transferase / Q000235:genetics*; D006689:Hodgkin Disease / Q000175:diagnosis* / Q000235:genetics*; D006801:Humans; D008297:Male; D008875:Middle Aged; D016017:Odds Ratio; D016133:Polymerase Chain Reaction; D011110:Polymorphism, Genetic; D011379:Prognosis; D012306:Risk; D013997:Time Factors
chemical_list: D005982:Glutathione Transferase