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Blood, 1 December 2004, Vol. 104, No. 12, pp. 3679-3687.
Prepublished online as a Blood First Edition Paper on June 29, 2004; DOI 10.1182/blood-2004-03-1154.
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NEOPLASIA
Gene expression profiling of pediatric acute myelogenous leukemia
Mary E. Ross,
Rami Mahfouz,
Mihaela Onciu,
Hsi-Che Liu,
Xiaodong Zhou,
Guangchun Song,
Sheila A. Shurtleff,
Stanley Pounds,
Cheng Cheng,
Jing Ma,
Raul C. Ribeiro,
Jeffrey E. Rubnitz,
Kevin Girtman,
W. Kent Williams,
Susana C. Raimondi,
Der-Cherng Liang,
Lee-Yung Shih,
Ching-Hon Pui, and
James R. Downing
From the Departments of Hematology-Oncology, Pathology, Biostatistics, and the Hartwell Center for Bioinformatics and Biotechnology, St Jude Children's Research Hospital, Memphis, TN; the Division of Pediatric Hematology-Oncology, Mackay Memorial Hospital, and the Division of Hematology-Oncology, Chang Gung Memorial Hospital, Taipei, Taiwan.
Contemporary treatment of pediatric acute myeloid leukemia (AML) requires the assignment of patients to specific risk groups. To explore whether expression profiling of leukemic blasts could accurately distinguish between the known risk groups of AML, we analyzed 130 pediatric and 20 adult AML diagnostic bone marrow or peripheral blood samples using the Affymetrix U133A microarray. Class discriminating genes were identified for each of the major prognostic subtypes of pediatric AML, including t(15;17)[PML-RAR ], t(8;21)[AML1-ETO], inv16 [CBF -MYH11], MLL chimeric fusion genes, and cases classified as FAB-M7. When subsets of these genes were used in supervised learning algorithms, an overall classification accuracy of more than 93% was achieved. Moreover, we were able to use the expression signatures generated from the pediatric samples to accurately classify adult de novo AMLs with the same genetic lesions. The class discriminating genes also provided novel insights into the molecular pathobiology of these leukemias. Finally, using a combined pediatric data set of 130 AMLs and 137 acute lymphoblastic leukemias, we identified an expression signature for cases with MLL chimeric fusion genes irrespective of lineage. Surprisingly, AMLs containing partial tandem duplications of MLL failed to cluster with MLL chimeric fusion gene cases, suggesting a significant difference in their underlying mechanism of transformation.

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