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Acute promyelocytic leukemia: From clinic to molecular biology

Acute promyelocytic leukemia (APL) is a good model for studying the human malignancies in that up to 90% of APL patients can achieve complete remission (CR) with a differentiation inducer, all‐trans retinoic acid (ATRA). APL is also associated with a specific chromosomal translocation t(15;17) which fuses the retinoic acid receptor α (RARα) gene with a chromosome 15q locus, PML. Recently the RARα and the PML gene structural alterations in t(15;17) have been characterized. The heterogeneity of the PML rearrangements juxtaposes different PML gene portions to the same set of RARα exons, producing two major PML‐RARα fusion mRNA isoforms. A retrotranscriptase/polymerase chain reaction (RT‐PCR) analysis of the fusion transcripts has been developed which allows the detection of minimal residual disease during the clinical remission of APL. Molecular study showed PML‐RARα can form heterodimers with wild‐type PML and RXR. Recently, PML has been shown to be one of the components of a nuclear body, POD. In APL, the normal organization of POD is disrupted by PML‐RARα, whereas ATRA treatment in vivo and in vitro can induce a reorganization of this organelle. Cytogenetic and molecular study allowed a variant translocation t(11;17) being recently discovered in a small subset of APL. This time RARα is fused to a new gene, PLZF, on chromosome 11q23. It has been shown that the PLZF‐RARα, like PML‐RARα, has a “dominant negative” effect on the wild‐type RAR‐RXR. Clinical data obtained from a group of t(11;17) APL patients showed that these respond poorly to ATRA and could be grouped in a special clinical syndrome within APL. The comparison of the biological activities mediated by PML‐RARα and PLZF‐RARα may give new insights into the pathogenesis as well as the mechanisms of ATRA‐induced differentiation in APL.