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Blood, 13 August 2009, Vol. 114, No. 7, pp. 1314-1318. Prepublished online as a Blood First Edition Paper on June 17, 2009; DOI 10.1182/blood-2008-12-193250. This Article Full Text (PDF) All Versions of this Article: blood-2008-12-193250v1 114/7/1314    most recent Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via CrossRef Google Scholar Articles by Stanulla, M. Articles by Schwab, M. PubMed PubMed Citation Articles by Stanulla, M. Articles by Schwab, M. Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted December 16, 2008 Accepted June 1, 2009 Thiopurine methyltransferase genetics is not a major risk factor for secondary malignant neoplasms after treatment of childhood acute lymphoblastic leukemia on Berlin-Frankfurt-Munster protocols Martin Stanulla*, Elke Schaeffeler, Anja Moricke, Sally A. Coulthard, Gunnar Cario, Andre Schrauder, Peter Kaatsch, Michael Dordelmann, Karl Welte, Martin Zimmermann, Alfred Reiter, Michel Eichelbaum, Hansjorg Riehm, Martin Schrappe, and Matthias Schwab University Children's Hospital, Kiel, Germany Dr Margarete Fischer-Bosch Institute of Clinical Pharmacology, Stuttgart, Germany Newcastle University, Northern Institute for Cancer Research, Newcastle upon Tyne, United Kingdom German Childhood Cancer Registry, IMBEI, Mainz, Germany Pediatric Hematology and Oncology, Hannover Medical School, Hannover, Germany Pediatric Hematology and Oncology, University Children's Hospital Giessen, Giessen, Germany Department of Clinical Pharmacology, University Hospital Tubingen, Tubingen, Germany * Corresponding author; email: martin.stanulla{at}uk-sh.de. 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 individuals 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 out of 129 patients who developed a secondary malignant neoplasm (SMN) after ALL treatment on seven consecutive German Berlin-Frankfurt-Munster (BFM) trials for all functionally relevant TPMT variants. Frequencies of TPMT variants were similarly distributed in SMN patients and the overall ALL patient population of 814 patients. Thus, TPMT does not play a major role in the etiology of SMN after treatment for childhood ALL according to BFM strategies. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this?

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