Acute promyelocytic leukemia (APL) originate from chromosomal translocations generating two types of fusion proteins both involving the retinoic acid receptor alpha (RAR alpha) 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.
[Acute promyelocytic leukemia, histone deacetylase, and response to retinoids]
1998-04 / vol 85 / pages 301-3
Humans; Antineoplastic Agents/therapeutic use; Tretinoin/therapeutic use; Histone Deacetylases/*metabolism; Leukemia, Promyelocytic, Acute/*drug therapy/*enzymology/genetics; Neoplasm Proteins/*metabolism; Oncogene Proteins, Fusion/*metabolism