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This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Leroy, H. Articles by Preudhomme, C. Search for Related Content PubMed PubMed Citation Articles by Leroy, H. Articles by Preudhomme, C. Related Collections Neoplasia Brief Reports Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  Blood, 15 May 2002, Vol. 99, No. 10, pp. 3848-3850 BRIEF REPORT Unlike AML1, CBF gene is not deregulated by point mutations in acute myeloid leukemia and in myelodysplastic syndromes Hugues Leroy, Christophe Roumier, Nathalie Grardel-Duflos, Elizabeth Macintyre, Pascale Lepelley, Pierre Fenaux, and Claude Preudhomme From the Laboratoire d'Hématologie A, Hôpital Calmette, and Service des Maladies du Sang, CHU Lille; Unité 524 INSERM, Institut de Recherche sur le Cancer de Lille; and Laboratoire d'Hématologie, Hôpital Necker enfants malades, Paris, France. The core-binding factor (CBF) complex is a heterodimeric transcription factor composed of 2 subunits, CBF and CBF, that play a major role in hematopoiesis. Both members of the CBF complex are frequently altered in acute myeloid leukemia (AML) by translocation, most commonly t(8;21), t(12;21), and t(3;21) for CBF, located in 21q22, and inv16(p13;q22) for CBF, located on 16q22. Recently, a new mechanism of alteration of CBF, by point mutation, has been reported in myeloid malignancies, particularly in M0 AML. In the present study, we found no point mutation of the CBF gene in 30 myelodysplastic syndromes and 100 AMLs, suggesting a limited role, if any, of CBF point mutations in those disorders. © 2002 by The American Society of Hematology.   CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: F. Dicker, C. Haferlach, W. Kern, T. Haferlach, and S. Schnittger Trisomy 13 is strongly associated with AML1/RUNX1 mutations and increased FLT3 expression in acute myeloid leukemia Blood, August 15, 2007; 110(4): 1308 - 1316. [Abstract] [Full Text] [PDF]

	Copyright © 2002 by American Society of Hematology         Online ISSN: 1528-0020