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 Printable version |
Acute promyelocytic leukemia, histone deacetylase and response to retinoïds |
Bulletin du Cancer. Volume 85, Number 4, 301, Avril 1998, Point sur…
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 Résumé
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Author(s) : Philippe Jeanteur |
Summary : Acute promyelocytic leukemia (APL) originate from chromosomal translocations generating two types of fusion proteins both involving the retinoic acid receptor (RAR) and either the gene PML (t(15;17)) or PLZF (t(11;17)). Recent publications cast a new light on the detailed molecular mechanism underlying the oncogenic activity of these fusion proteins which block myeloid terminal differentiation by recruiting histone deacetylases to the promoters of target genes through co-repressor proteins. They also explain the different responses to treatment by all-trans retinoic acid (ATRA) of these two variants which are otherwise clinically indistinguishable. |
Keywords : retinoic acid receptors (RAR), retinoic acid, fusion proteins, chromosomal translocations, trichostatin A. |
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