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Blood, 1 March 2006, Vol. 107, No. 5, pp. 1806-1809.
Prepublished online as a Blood First Edition Paper on November 15, 2005; DOI 10.1182/blood-2005-08-3408.
 Previous Article | Next Article 
Submitted August 24, 2005
Accepted October 20, 2005
KIT mutations, and not FLT3 internal tandem duplication, are strongly associated with a poor prognosis in pediatric acute myeloid leukemia with t(8;21): a study of the Japanese Childhood AML Cooperative Study Group
Akira Shimada, Tomohiko Taki, Ken Tabuchi, Akio Tawa, Keizo Horibe, Masahiro Tsuchida, Ryoji Hanada, Ichiro Tsukimoto, and Yasuhide Hayashi*
Department of Hematology/Oncology, Gunma Children's Medical Center, Seta, Gunma, Japan
Department of Molecular Laboratory Medicine, Kyoto Prefectural University of Medicine Graduate School of Medical Science, Kyoto, Japan
Department of Hematology, Kanagawa Children's Medical Center, Yokohama, Kanagawa, Japan
Department of Pediatrics, National Hospital Organization Osaka National Hospital, Osaka, Japan
Clinical Research Center, National Hospital Organization Nagoya Medical Center, Nagoya, Japan
Department of Pediatrics, Ibaraki Children's Hospital, Mito, Ibaraki, Japan
Division of Hematology/Oncology, Saitama Children's Medical Center, Saitama, Japan
Department of the First Pediatrics, Toho University School of Medicine, Omori, Tokyo, Japan
* Corresponding author; email: hayashiy-tky{at}umin.ac.jp.
t(8;21)-acute myeloid leukemia (AML) patients are considered to have a good prognosis; however, ~50% of them relapse. The genetic alterations associated with a worse outcome in t(8;21)-AML remained unknown. Recently, aberrations of receptor tyrosine kinases (RTKs) were frequently found in AML patients. However, the prevalence and prognostic impact of RTK aberrations in pediatric t(8;21)-AML remains undetermined. Here, we found the kinase domain mutations of the KIT gene in 8 (17.4%) of 46 t(8;21)-AML patients among newly diagnosed pediatric AML patients treated on the AML99 protocol in Japan. Significant differences between patients with or without KIT mutations were observed in the 4-year overall survival (50.0% vs. 97.4%, p=0.001), disease free survival (37.5% vs. 94.7%, p< 0.00001) and relapse rate (47.0% vs. 2.7%, p< 0.000001). Furthermore, FLT3-internal tandem duplication was found in only 2 (4.3%) patients. These results suggested that KIT mutations are strongly associated with a poor prognosis in pediatric t(8;21)-AML.
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