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

被引:61
作者
Chapiro, Elise
Russell, Lisa
Radford-Weiss, Isabelle
Bastard, Christian
Lessard, Michel
Struski, Stephanie
Cave, Helene
Fert-Ferrer, Sandra
Barin, Carole
Maarek, Odile
Della-Valle, Veronique
Strefford, Jonathan C.
Berger, Roland
Harrison, Christine J.
Bernard, Olivier A.
Nguyen-Khac, Florence
机构
[1] Grp Hosp Pitie Salpetriere, Serv Hematol Biol, AP HP, F-75013 Paris, France
[2] INSERM, Paris, France
[3] Univ Paris 06, Paris, France
[4] Univ Southampton, Leukaemia Res Cytogenet Grp, Canc Sci Div, Southampton, Hants, England
[5] Univ Paris 05, Paris, France
[6] Hop Necker Enfants Malad, Lab Cytogenet, AP HP, Paris, France
[7] Lab Genet Oncol, Rouen, France
[8] Hop Hautepierre, Hematol Lab, Strasbourg, France
[9] Hop Robert Debre, AP HP, Biochim Genet Lab, F-75019 Paris, France
[10] Genet Lab, Chambery, France
[11] Genet Lab, Tours, France
[12] Hop St Louis, AP HP, Hematol Lab, Paris, France
关键词
D O I
10.1182/blood-2006-03-010835
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
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 post-translational 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.
引用
收藏
页码:3560 / 3563
页数:4
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