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Abstract
Acute promyelocytic leukemia (APIL) results from a malignant process that leads to the accumulation in the blood and the bone marrow of myeloid precursor cells characterized by an abnormal behavior and a differentiation arrest. It aroused considerable interest well beyond the hematologic field during the last five years since APL has two unique features i) the remission of the disease obtained with all-trans retinoic acid (ATRA) treatment ii) the presence in APL blasts of an abnormal protein, the promyelocytic myeloid leukemia/retinoic acid receptor (PML/RARα) protein. APL is characterized cytogenetically by a t(15;17) translocation which involves both the PML gene on chromosome 15 and the: RARα gene on chromosome 17 and gives rise to the PML/RARα fusion protein.