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 α gene are commonly associated with development of acute promyelocytic leukemia. Through the development of transgenic mouse models, some retinoic acid receptor α 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.

Original languageEnglish
Pages (from-to)206-211
Number of pages6
JournalCurrent opinion in hematology
Issue number4
StatePublished - 2001


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