ACUTE PROMYELOCYTIC LEUKEMIA, HISTONE DEA CETYLASE AND RESPONSE TO RETINOIDS

Acute promyelocytic leukemia (APL) originate from chromosomal transloc ations generating two types of fusion proteins both involving the reti noic 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 det ailed molecular mechanism underlying the oncogenic activity of these f usion proteins which block myeloid terminal differentiation by recruit ing histone deacetylases to the promoters of target genes through co-r epressor proteins. They also explain the different response to treatme nt by all-trans retinoic acid (ATRA) of these two variants which are o therwise clinically indistinguishable.