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Overexpression of CEBPA resulting from the translocation t(14;19)(q32;q13) of human precursor B acute lymphoblastic leukemia

Lookup NU author(s): Dr Lisa Russell, Professor Christine Harrison FRCPath FMedSci

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Abstract

Subtle variation in the expression or function of a small group of transcription factors can drive leukemogenesis. The CEBPA protein is known to regulate the balance between cell proliferation and differentiation during early hematopoietic development and myeloid differentiation. In human myeloid leukemia, CEBPA is frequently inactivated by mutation and indirect and posttranslational mechanisms, in keeping with tumor suppressor properties. We report that CEBPA is activated by juxtaposition to the immunoglobulin gene enhancer upon its rearrangement with the immunoglobulin heavy-chain locus in precursor B-cell acute lymphoblastic leukemia harboring t(14;19)(q32;q13). Overexpression of apparently normal CEBPA RNA or protein was observed in 6 patients. These data indicate that CEBPA may exhibit oncogenic as well as tumor suppressor properties in human leukemogenesis.

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Author(s): Chapiro E, Russell LJ, Radford-Weiss I, Bastard C, Lessard M, Struski S, Cave H, Fert-Ferrer S, Barin C, Maarek O, Della-Valle V, Strefford JC, Berger R, Harrison CJ, Bernard OA, Nguyen-Khac F

Publication type: Article

Publication status: Published

Journal: Blood

Year: 2006

Volume: 108

Issue: 10

Pages: 3560-3563

ISSN (print): 0006-4971

ISSN (electronic): 1528-0020

URL: http://dx.doi.org/10.1182/blood-2006-03-010835

DOI: 10.1182/blood-2006-03-010835

Notes: Journal Article Research Support, Non-U.S. Gov't United States

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