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The theory of APL

Oncogene volume 20, pages 7216–7222 (2001)Cite this article

Abstract

Acute promyelocytic leukemia (APL) is associated with reciprocal and balanced chromosomal translocations always involving the Retinoic Acid Receptor α (RARα) gene on chromosome 17 and variable partner genes (X genes) on distinct chromosomes. RARα fuses to the PML gene in the vast majority of APL cases, and in a few cases to the PLZF, NPM, NuMA and STAT5b genes. As a consequence, X-RARα and RARα-X fusion genes are generated encoding aberrant fusion proteins that can interfere with X and/or RARα function. Here we will review the relevant conclusions and the open questions that stem from a decade of in vivo analysis of APL pathogenesis in the mouse in transgenic and knock-out models.

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Acknowledgements

This work is supported by the NCI, the De Witt Wallace Fund for Memorial Sloan-Kettering Cancer Center, the Mouse Model of Human Cancer Consortium (MMHCC) and NIH Grants to PP Pandolfi and the Lymphoma & Leukemia Society of which PP Pandolfi is a Scholar. Finally, we are indebted to all the past and present members of the laboratory of Molecular and Developmental Biology (MADB) at the Memorial Sloan-Kettering Cancer Center, working on APL and related subjects.

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  1. Department of Pathology, Sloan-Kettering Division, Molecular Biology Program, Memorial Sloan-Kettering Cancer Center, Graduate School of Medical Sciences, Cornell University, 1275 York Avenue, New York, NY 10021, New York, USA

    Francesco Piazza, Carmela Gurrieri & Pier Paolo Pandolfi

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  1. Francesco Piazza
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  2. Carmela Gurrieri
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  3. Pier Paolo Pandolfi
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Correspondence to Pier Paolo Pandolfi.

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Piazza, F., Gurrieri, C. & Pandolfi, P. The theory of APL. Oncogene 20, 7216–7222 (2001). https://doi.org/10.1038/sj.onc.1204855

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