Thiopurine methyltransferase genetics is not a major risk factor for secondary malignant neoplasms after treatment of childhood acute lymphoblastic leukemia on Berlin-Frankfurt-Münster protocols
Date
2009
Authors
Stanulla, M.
Schaeffeler, E.
Moricke, A.
Coulthard, S.
Cario, G.
Schrauder, A.
Kaatsch, P.
Dordelmann, M.
Welte, K.
Zimmerman, M.
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Journal article
Citation
Blood, 2009; 114(7):1314-1318
Statement of Responsibility
Martin Stanulla, Elke Schaeffeler, Anja Möricke, Sally A. Coulthard, Gunnar Cario, André Schrauder, Peter Kaatsch, Michael Dördelmann, Karl Welte, Martin Zimmermann, Alfred Reiter, Michel Eichelbaum, Hansjörg Riehm, Martin Schrappe, and Matthias Schwab
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Abstract
Thiopurine methyltransferase (TPMT)is involved in the metabolism of thiopurines such as 6-mercaptopurine and 6-thioguanine. TPMT activity is significantly altered by genetics, and heterozygous and even more homozygous variant people reveal substiantially decreased TPMT activity. Treatment for childhood acute lymphoblastic leukemia (ALL) regularly includes the use of thiopurine drugs. Importantly, childhood ALL patients with low TPMT activity have been considered to be at increased risk of developing therapy-associated acute myeloid leukemia and brain tumors. In the present study, we genotyped 105 of 129 patients who developed a secondary malignant neoplasm after ALL treatment on 7 consecutive German Berlin-Frankfurt-Münster trials for all functionally relevant TPMT variants. Frequencies of TPMT variants were similarly distributed in secondary malignant neoplasm patients and the overall ALL patient population of 814 patients. Thus, TPMT does not play a major role in the etiology of secondary malignant neoplasm after treatment for childhood ALL, according to Berlin-Frankfurt-Münster strategies.
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© 2009 by The American Society of Hematology