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 |