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Human Molecular Genetics, 2001, Vol. 10, No. 7 769-775
© 2001 Oxford University Press

Oncogenes and tumor suppressors in the molecular pathogenesis of acute promyelocytic leukemia

Pier Paolo Pandolfi+

Department of Human Genetics and Molecular Biology Program, Memorial Sloan-Kettering Cancer Center, 1275 York Avenue, New York, NY 10021, USA

Acute promyelocytic leukemia (APL) is associated with reciprocal chromosomal translocations always involving the retinoic acid receptor {alpha} (RAR{alpha}) gene on chromosome 17 and variable partner genes (X genes) on distinct chromosomes. RAR{alpha} 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, respectively, leading to the generation of RAR{alpha}–X and X–RAR{alpha} fusion genes. Both fusion proteins can exert oncogenic functions through their ability to interfere with the activities of X and RAR{alpha} proteins. Here, it will be discussed in detail how an extensive biochemical analysis as well as a systematic in vivo genetic approach in the mouse has allowed the definition of the multiple oncogenic activities of PML–RAR{alpha}, and how it has become apparent that this oncoprotein is able to impair RAR{alpha} at the transcription level and the tumor suppressive function of the PML protein.

+ Tel: +1 212 639 6168; Fax: +1 212 717 3374; Email: p-pandolfi@ski.mskcc.org


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