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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.
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CLINICAL TRIALS AND OBSERVATIONS
Brief report
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
From the Department of Hematology/Oncology, Gunma Children's Medical Center, Gunma; the Department of Molecular Laboratory Medicine, Kyoto Prefectural University of Medicine Graduate School of Medical Science, Kyoto; the Department of Hematology, Kanagawa Children's Medical Center, Yokohama, Kanagawa; the Department of Pediatrics, National Hospital Organization Osaka National Hospital, Osaka; the Clinical Research Center, National Hospital Organization Nagoya Medical Center, Nagoya; the Department of Pediatrics, Ibaraki Children's Hospital, Ibaraki; the Division of Hematology/Oncology, Saitama Children's Medical Center, Saitama; and the Department of First Pediatrics, Toho University School of Medicine, Omori, Tokyo, Japan.
Patients with t(8;21) acute myeloid leukemia (AML) are considered to have a good prognosis; however, approximately 50% of them relapse. The genetic alterations associated with a poor outcome in t(8;21) AML remain unknown. Recently, aberrations of receptor tyrosine kinases (RTKs) were frequently found in patients with AML. 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 patients with t(8;21) AML among newly diagnosed pediatric patients with AML 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% versus 97.4%, P = .001), disease-free survival (37.5% versus 94.7%, P < .001) and relapse rate (47.0% versus 2.7%, P < .001). 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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