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Blood, 1 October 2006, Vol. 108, No. 7, pp. 2416-2419. Prepublished online as a Blood First Edition Paper on June 20, 2006; DOI 10.1182/blood-2006-02-003582. This Article Full Text Full Text (PDF) All Versions of this Article: blood-2006-02-003582v1 108/7/2416    most recent 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 Lee, Y.-J. Articles by Kogan, S. C. Search for Related Content PubMed PubMed Citation Articles by Lee, Y.-J. Articles by Kogan, S. C. Related Collections Neoplasia Oncogenes and Tumor Suppressors Gene Expression Brief Reports Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  NEOPLASIA Brief report CCAAT/enhancer binding proteins alpha and epsilon cooperate with all-trans retinoic acid in therapy but differ in their antileukemic activities Young-Jin Lee, Letetia C. Jones, Nikolai A. Timchenko, Danilo Perrotti, Daniel G. Tenen, and Scott C. Kogan From the Department of Laboratory Medicine and Comprehensive Cancer Center, University of California San Francisco; Huffington Center on Aging and Department of Pathology, Baylor College of Medicine, Houston, TX; Department of Molecular Virology, Immunology and Medical Genetics and the Comprehensive Cancer Center, The Ohio State University, Columbus; and Harvard Institutes of Medicine, Harvard Medical School, Boston, MA. CCAAT/enhancer binding proteins (C/EBPs) play critical roles in myelopoiesis. Dysregulation of these proteins likely contributes to the pathogenesis of myeloid disorders characterized by a block in granulopoiesis. In one such disease, acute promyelocytic leukemia (APL), a promyelocytic leukemia–retinoic acid receptor (PML-RAR) fusion protein is expressed as a result of a t(15;17) chromosomal translocation. Treatment of PML-RAR leukemic cells with all-trans retinoic acid (ATRA) causes them to differentiate into mature neutrophils, an effect thought to be mediated by C/EBPs. In this study, we assess the potential for cooperativity between increased C/EBP activity and ATRA therapy. We demonstrate that although both C/EBP and C/EBP can significantly prolong survival in a mouse model of APL, they are not functionally equivalent in this capacity. We also show that forced expression of C/EBP or C/EBP in combination with ATRA treatment has a synergistic effect on survival of leukemic mice compared with either therapy alone. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: T. Pabst and B. U. Mueller Complexity of CEBPA Dysregulation in Human Acute Myeloid Leukemia Clin. Cancer Res., September 1, 2009; 15(17): 5303 - 5307. [Abstract] [Full Text] [PDF] S. Koschmieder, B. Halmos, E. Levantini, and D. G. Tenen Dysregulation of the C/EBP{alpha} Differentiation Pathway in Human Cancer J. Clin. Oncol., February 1, 2009; 27(4): 619 - 628. [Abstract] [Full Text] [PDF]

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