The theory of APL Journal Article


Authors: Piazza, F.; Gurrieri, C.; Pandolfi, P. P.
Article Title: The theory of APL
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.
Keywords: pathogenesis; review; animals; mice; mice, knockout; animal model; mitogenesis; transgenic mouse; animalia; mus musculus; mice, transgenic; cell transformation, neoplastic; leukemia, promyelocytic, acute; hybrid protein; leukemogenesis; acute myeloblastic leukemia; oncogene proteins, fusion; chromosome translocation; translocation, genetic; heterozygosity loss; disease models, animal; stat5 protein; retinoic acid; chromosome 17; knockout mouse; transgenic mice; animal models; retinoic acid receptor; receptors, retinoic acid; apl; humans; priority journal; chromosome translocation 15; ko mice; tumor metamorphosers
Journal Title: Oncogene
Volume: 20
Issue: 49
ISSN: 0950-9232
Publisher: Nature Publishing Group  
Date Published: 2001-10-29
Start Page: 7216
End Page: 7222
Language: English
DOI: 10.1038/sj.onc.1204855
PUBMED: 11704849
PROVIDER: scopus
DOI/URL:
Notes: Export Date: 21 May 2015 -- Source: Scopus
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  1. Francesco Piazza
    13 Piazza