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Abstract The association of exagerated haemorrhagic syndrome with certain leukaemia was first described by French hematologist in 1949. Hillstad (1957), bestowed the appellation promylocytic leukemia upon this morphologic clinical syndrome of AML (Crozat and Favre,1949). The promyelocytic leukemia (M3) subtype accounts for 5- 10% of all cases of AML. Two morphologic variants of APL are identified, a hyper-granular (M3) and Microgranular variant. Both are strongly preoxidase and sudan black positive, give positive reaction with CD13, CD33 and negative with HLA-DRand CD34 {Miller and Daoust, 2000). APL is found to be consistently associated with a balanced translocation t(15 ; 17) which results in the formation of PML-RARa. chimeric products (Biondi et al.,1992). This chimeric product on one hand induces an arrest of differentiation of the granulocytic lineage through an abnormal RARa., and on the other hand alters the cell cycle and the nuclear biology through an abnormal PML with subsequent expansion of the population of leukemic promyelocyte (Degos, 1999). The advert of differentiation therapy with all -trans retinoic acid (ATRA) paved the way for the design of modern diagnostic strategies. |