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Originally published as JCO Early Release 10.1200/JCO.2008.21.6135 on March 9 2009 © 2009 American Society of Clinical Oncology.
In ReplyDivision of Hematology and Oncology, Department of Internal Medicine; and Department of Microbiology, Virology, Immunology, and Medical Genetics, Comprehensive Cancer Center, The Ohio State University, Columbus, OH
Division of Hematology and Oncology, Department of Internal Medicine, The Ohio State University, Columbus, OH; and The Cancer and Leukemia Group B Statistical Center, Duke University Medical Center, Durham, NC
Division of Hematology and Oncology, Department of Internal Medicine, The Ohio State University, Columbus, OH We agree with Dr Medeiros1 that the data reported by Wouters et al2 at the 2008 American Society of Hematology Meeting showing that the prognostic impact of CEBPA mutations might be restricted to double-mutant patients are interesting, and several groups are currently investigating this. We also agree that it would be interesting to assess the prognostic impact of CEBPA mutations within subsets of patients with cytogenetically normal acute myeloid leukemia and molecular high-risk disease (ie, FLT3 internal tandem duplication [FLT3-ITD], or NPM1 wild type [wt], or both). Among the subset of patients with NPM1wt but without FLT3-ITD, we observed that CEBPA mutations conferred a better prognosis, with the 5-year event-free survival rates for 21 patients with CEBPA mutations of 62% v 13% for 24 patients with CEBPAwt (P = .0003). However, the assessment of the subset with FLT3-ITD is difficult because of the small number of patients harboring both FLT3-ITD and CEBPA mutations in our patient set—there were only eight such patients.3 When these patients were compared with those with FLT3-ITD and CEBPAwt (n = 62), the 5-year event-free survival rates were 38% and 19%, respectively, but the difference was not statistically significant (P = .44). Thus, whereas CEBPA mutations seem to affect favorably the outcome of the patients with molecular high-risk cytogenetically normal acute myeloid leukemia without FLT3-ITD, a larger set of patients harboring FLT3-ITD and CEBPA mutations needs to be analyzed before definitive conclusions as to the prognostic significance of CEBPA mutations in FLT3-ITD–positive patients can be drawn. AUTHORS' DISCLOSURES OF POTENTIAL CONFLICTS OF INTEREST The author(s) indicated no potential conflicts of interest. REFERENCES
1. Medeiros BC: Role of CEBPA in normal karyotype acute myeloid leukemia. J Clin Oncol 27:2105; 2009. 2. Wouters BJ, Erpelinck-Verschueren CAJ, Lowenberg B, et al: Double, but not single, CEBPA mutations define a subgroup of acute myeloid leukemia with favorable outcome and a distinct gene expression profile. Blood 112:58; 2008 abstr 141. 3. Marcucci G, Maharry K, Radmacher MD, et al: Prognostic significance of, and gene and microRNA expression signatures associated with, CEBPA mutations in cytogenetically normal acute myeloid leukemia with high-risk molecular features: A Cancer and Leukemia Group B study. J Clin Oncol 26:5078–5087, 2008.
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Copyright © 2009 by the American Society of Clinical Oncology, Online ISSN: 1527-7755. Print ISSN: 0732-183X
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