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

نویسندگان

  • Elise Chapiro
  • Lisa Russell
  • Isabelle Radford-Weiss
  • Christian Bastard
  • Michel Lessard
  • Stephanie Struski
  • Helene Cave
  • Sandra Fert-Ferrer
  • Carole Barin
  • Odile Maarek
  • Veronique Della-Valle
  • Jonathan C Strefford
  • Roland Berger
  • Christine J Harrison
  • Olivier A Bernard
  • Florence Nguyen-Khac
چکیده

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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عنوان ژورنال:
  • Blood

دوره 108 10  شماره 

صفحات  -

تاریخ انتشار 2006