Abstract
Acute Promyelocytic Leukemia (APL) is a distinct subset of acute myeloid leukemia (AML) (FAB-M3 according to the French-American-British Cooperative Group). It is morphologically distinguished by the presence of hyper-granular leukemic blasts (Sultan et al. 1973; Bennett et al. 1976). The clinical propensity of APL patients to hemorrhage, the feature that first drew the attention to this type of acute leukemia, is thought to be due to the release of procoagulants by the granules in the malignant promyelocytes (Gralnick and Abrell 1973; Falanga et al. 1988). APL are cytogenetically distinguished by a balanced reciprocal chromosome 15; 17 translocation- t(15;17) (Rowley et al. 1977; Mitelman 1988). The high frequency (70 to 100% of cases) and the tumor-type specificity of the t(15;17) suggest that chromosome break-points affect DNA sequence that might be crucial in the pathogenesis of this malignancy.
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© 1993 Springer-Verlag Berlin · Heidelberg
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Biondi, A. et al. (1993). Molecular Genetics of the t(15;17) Translocation in Acute Promyelocytic Leukemia. In: Ludwig, WD., Thiel, E. (eds) Recent Advances in Cell Biology of Acute Leukemia. Recent Results in Cancer Research, vol 131. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-84895-7_31
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DOI: https://doi.org/10.1007/978-3-642-84895-7_31
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