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Fusion of AML1/Runx1 to Copine VIII, a novel member of the copine family, in an aggressive acute myelogenous leukemia with t(12;21) translocation

Leukemia volume 17, pages 1665–1666 (2003)Cite this article

TO THE EDITOR

Normal acute myeloid leukemia (AML)1 (also Runx1 and CBFalpha2) interacts with core binding factor CBF beta to function as a heterodimeric transcriptional activator called CBF. CBF is a master regulator of the genetic cascade responsible for myeloid differentiation.1 Hematopoietic targets for CBF activation include IL-3, GM-CSF, M-CSF receptor, and myeloperoxidase.1 In the absence of either component of CBF, there is a general failure of embryonic definitive hematopoiesis.1

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Authors and Affiliations

  1. Indiana University Cancer Center and Walther Oncology Center, Indianapolis, IN, USA

    H Ramsey & R Hromas

  2. The Scripps Research Institute, La Jolla, CA, USA

    Do-E Zhang

  3. Genzyme Genetics, Santa Fe, NM, USA

    K Richkind

  4. Cancer Centers of America, SW Medical Center, OK, USA

    A Burcoglu-O'Ral

Authors
  1. H Ramsey
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  2. Do-E Zhang
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  5. R Hromas
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Ramsey, H., Zhang, DE., Richkind, K. et al. Fusion of AML1/Runx1 to Copine VIII, a novel member of the copine family, in an aggressive acute myelogenous leukemia with t(12;21) translocation. Leukemia 17, 1665–1666 (2003). https://doi.org/10.1038/sj.leu.2403048

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