Mouse models of acute promyelocytic leukemia

Curr Opin Hematol. 2001 Jul;8(4):206-11. doi: 10.1097/00062752-200107000-00005.


Translocations involving a variety of fusion partners, such as promyelocytic leukemia gene, promyelocytic leukemia zinc finger, nucleophosmin, nuclear matrix protein, and signal transducer and activator of transcription protein 5B, with the retinoic acid receptor alpha gene are commonly associated with development of acute promyelocytic leukemia. Through the development of transgenic mouse models, some retinoic acid receptor alpha translocation fusion proteins have been shown to be capable of initiating acute promyelocytic leukemia development, and dictate the leukemias' responsiveness to retinoic acid. Transgenic mouse models also have identified the influence of reciprocal translocation fusion proteins on acute promyelocytic leukemia development, and have demonstrated that additional mutations can contribute to the development of acute promyelocytic leukemia. In this review, the authors summarize current mouse models of acute promyelocytic leukemia and describe current knowledge about additional genetic alterations that occur during development of acute promyelocytic leukemia in the mouse.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.
  • Review

MeSH terms

  • Animals
  • Antineoplastic Agents / therapeutic use
  • Arsenic / therapeutic use
  • Chromosome Deletion
  • Disease Models, Animal*
  • Leukemia, Promyelocytic, Acute / drug therapy
  • Leukemia, Promyelocytic, Acute / genetics*
  • Mice
  • Models, Biological
  • Mutation
  • Neoplasm Proteins / physiology
  • Oncogene Proteins, Fusion / physiology
  • Tretinoin / therapeutic use


  • Antineoplastic Agents
  • Neoplasm Proteins
  • Oncogene Proteins, Fusion
  • PLZF-RARalpha fusion protein, mouse
  • promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein
  • Tretinoin
  • Arsenic