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 Blood, 15 November 2008, Vol. 112, No. 10, pp. 4193-4201.
Prepublished online as a Blood First Edition Paper on August 20, 2008; DOI 10.1182/blood-2008-02-134411.

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NEOPLASIA

An 86-probe-set gene-expression signature predicts survival in cytogenetically normal acute myeloid leukemia

Klaus H. Metzeler1, Manuela Hummel2, Clara D. Bloomfield3, Karsten Spiekermann1,4, Jan Braess1, Maria-Cristina Sauerland5, Achim Heinecke5, Michael Radmacher3,6, Guido Marcucci3, Susan P. Whitman3, Kati Maharry3,6, Peter Paschka3,7, Richard A. Larson8, Wolfgang E. Berdel9, Thomas Büchner9, Bernhard Wörmann10, Ulrich Mansmann2, Wolfgang Hiddemann1,4, Stefan K. Bohlander1,4, Christian Buske1,4, for Cancer and Leukemia Group B and the German AML Cooperative Group

1 Laboratory of Leukemia Diagnostics, Department of Internal Medicine III, Ludwig-Maximilians-Universität, Campus Groβhadern and 2 Institute for Medical Informatics, Biometry and Epidemiology, Ludwig-Maximilians-Universität, Munich, Germany; 3 Division of Hematology and Oncology, Department of Internal Medicine, Comprehensive Cancer Center, Ohio State University, Columbus; 4 Clinical Cooperative Group Leukemia, Helmholtz Zentrum München-National Research Centre for Environment and Health, Munich, Germany; 5 Department of Medical Informatics and Biomathematics, University of Münster, Münster, Germany; 6 Cancer and Leukemia Group B Statistical Center, Durham, NC; 7 Department of Internal Medicine II, J. W. Goethe-Universität, Frankfurt am Main, Germany; 8 University of Chicago, IL; 9 Department of Internal Medicine A, Hematology and Oncology, University of Münster, Münster, Germany; and 10 Department of Hematology and Oncology, Municipal Hospital, Braunschweig, Germany

Patients with cytogenetically normal acute myeloid leukemia (CN-AML) show heterogeneous treatment outcomes. We used gene-expression profiling to develop a gene signature that predicts overall survival (OS) in CN-AML. Based on data from 163 patients treated in the German AMLCG 1999 trial and analyzed on oligonucleotide microarrays, we used supervised principal component analysis to identify 86 probe sets (representing 66 different genes), which correlated with OS, and defined a prognostic score based on this signature. When applied to an independent cohort of 79 CN-AML patients, this continuous score remained a significant predictor for OS (hazard ratio [HR], 1.85; P = .002), event-free survival (HR = 1.73; P = .001), and relapse-free survival (HR = 1.76; P = .025). It kept its prognostic value in multivariate analyses adjusting for age, FLT3 ITD, and NPM1 status. In a validation cohort of 64 CN-AML patients treated on CALGB study 9621, the score also predicted OS (HR = 4.11; P < .001), event-free survival (HR = 2.90; P < .001), and relapse-free survival (HR = 3.14, P < .001) and retained its significance in a multivariate model for OS. In summary, we present a novel gene-expression signature that offers additional prognostic information for patients with CN-AML.


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