TY - JOUR
T1 - Increased risk for treatment-related mortality after bone marrow transplantation in GSTM1-positive recipients
AU - Terakura, S.
AU - Murata, M.
AU - Nishida, T.
AU - Emi, N.
AU - Akatsuka, Y.
AU - Morishima, Y.
AU - Kodera, Y.
AU - Naoe, T.
N1 - Funding Information:
We thank the staff of transplant and donor centers, and JMDP. We also thank Dr Stanley R Riddell for critical reading of the manuscript. This work was supported by a grant from the Ministry of Health, Labour and Welfare of Japan (MM and YK).
PY - 2006/2
Y1 - 2006/2
N2 - Treatment-related mortality (TRM) is a major obstacle to successful allogeneic hematopoietic stem cell transplantation (HSCT). A variety of drugs are used in allogeneic HSCT, and a genetic polymorphism in metabolic enzymes could affect the metabolism of drugs and potentially influence TRM. Here, we focused attention on GSTM1 and GSTT1 enzymes, which metabolize chemotherapeutic agents, chemical carcinogens and by-products of oxidative stress and are absent from more than 50% of some populations. To assess the significance of homozygous GSTM1 and GSTT1 gene deletion in HSCT, we analyzed DNA from 373 patients with hematological disease and their HLA-identical unrelated bone marrow donors using PCR. Homozygous GSTM1 and GSTT1 gene deletions were observed in 56 and 45% of patients, respectively, and 57 and 46% of donors, respectively. There was no significant association between GSTT1 polymorphism and any outcome. However, a GSTM1-positive genotype in recipients was significantly associated with higher TRM and lower survival. These results suggest that a GSTM1-null genotype in recipients protects against TRM after allogeneic HSCT. Further studies are needed to elucidate a mechanism of increased risk for TRM in GSTM1-positive recipients.
AB - Treatment-related mortality (TRM) is a major obstacle to successful allogeneic hematopoietic stem cell transplantation (HSCT). A variety of drugs are used in allogeneic HSCT, and a genetic polymorphism in metabolic enzymes could affect the metabolism of drugs and potentially influence TRM. Here, we focused attention on GSTM1 and GSTT1 enzymes, which metabolize chemotherapeutic agents, chemical carcinogens and by-products of oxidative stress and are absent from more than 50% of some populations. To assess the significance of homozygous GSTM1 and GSTT1 gene deletion in HSCT, we analyzed DNA from 373 patients with hematological disease and their HLA-identical unrelated bone marrow donors using PCR. Homozygous GSTM1 and GSTT1 gene deletions were observed in 56 and 45% of patients, respectively, and 57 and 46% of donors, respectively. There was no significant association between GSTT1 polymorphism and any outcome. However, a GSTM1-positive genotype in recipients was significantly associated with higher TRM and lower survival. These results suggest that a GSTM1-null genotype in recipients protects against TRM after allogeneic HSCT. Further studies are needed to elucidate a mechanism of increased risk for TRM in GSTM1-positive recipients.
UR - http://www.scopus.com/inward/record.url?scp=32844469196&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=32844469196&partnerID=8YFLogxK
U2 - 10.1038/sj.bmt.1705257
DO - 10.1038/sj.bmt.1705257
M3 - Article
C2 - 16415899
AN - SCOPUS:32844469196
SN - 0268-3369
VL - 37
SP - 381
EP - 386
JO - Bone Marrow Transplantation
JF - Bone Marrow Transplantation
IS - 4
ER -