P = 0.0353 (according to two-sided Fisher’s exact test). The analysis of NAT2 revealed no significant differences between controls and any patient subgroup. ![]() Patients were sub-grouped according to cytogenetics (normal, non-complex, complex) and in t-AML/MDS according to primary malignancy (Hodgkin’s lymphoma (HL), non-Hodgkin’s lymphoma (NHL) and breast cancer). NAT2-polymorphisms (fast metabolisers, heterozygotes and slow metabolisers) were analysed in 352 patients (196 AML, 156 MDS, 28 t-AML/MDS) and compared with 240 controls. The polymorphisms of GSTT1 and GSTM1 were examined in 439 patients (265 AML, 174 MDS, 65 t-AML/MDS) and compared with 248 healthy controls. Data were compared with the results of 266 healthy controls. ![]() GSTP1-poymorphisms were analysed in blood samples or bone marrow of 326 patients (180 AML, 146 MDS) of whom 65 had therapy-related malignancies (t-AML/t-MDS) by PCR/RFLP analysis. To extend our database by a higher number of individuals examined and by determining the occurrence of NAT2and two GSTP1-polymorphisms (Exon 5: Ile105Val and Exon 6: Ala114Val). Recently, our group could demonstrate a significantly increased risk for t-AML/MDS after breast cancer-therapy in individuals with a double deletion of GSTT1 and GSTM1. Thus, further efforts are needed to clarify the relevance of polymorphisms of metabolising enzymes for the pathogenesis of de novo and secondary malignancies. ![]() Recent studies examined the role of these enzymes in carcino- and leukemogenesis. Trümper Department of Hematologgy/Oncology, University of Göttingen, Robert-Koch-Strasse 40, 37075 Göttingen, Germany ∗ E-mail: Glutathione S-transferases (GST) and N-acetyltransferases metabolise exogenous and endogenous compounds. Leukemia Research 27 Supplement Numer 1 (2003) S1–S123ħth International Symposium on Myelodysplastic Syndromes-Abstracts EPIDEMIOLOGY POLYMORPHISMS OF METABOLIZING ENZYMES (NAT2, GSTT1, GSTM1 AND GSTP1) IN DE NOVO AND THERAPY-INDUCED MDS AND AML D.
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