ISSN: 1939-067X

Journal of Experimental Stroke & Translational Medicine

Myelogenous Leukemia Journals

 Chronic myelogenous leukemia (CML) is the prototype of the myeloproliferative disorders (See table below). The myeloproliferative disorders are characterized by an overproduction of at least 1 cell lineage (ie, granulocytic, megakaryocytic, erythroid, and/or monocytic), a subacute to chronic course, and a tendency to evolve into a more aggressive lethal form. The chronic myeloproliferative disorders differ from acute leukemias clinically by a less acute course and morphologically by maturation of the neoplastic clone. Numerous blasts typical of acute leukemia are not seen in the myeloproliferative syndromes unless transformation has occurred. The myelodysplastic syndromes are distinguished by ineffective hematopoiesis leading to cytopenias rather than the overproduction of cells seen in the myeloproliferative syndromes. Myelodysplasias are also associated with different cytogenetic abnormalities. CML is the most common of the myeloproliferative syndromes and the best characterized with regard to molecular abnormalities, resulting from a clonal expansion of cells with a Philadelphia chromosome producing a distinctive breakpoint cluster region— Abelson leukemia virus (BCR-ABL) fusion gene product. Karyotypic or molecular detection of the classic translocation, t(9;22)(q34q11), known as the Philadelphia chromosome or BCR-ABL fusion product, is not only essential in the diagnosis of CML, but useful in monitoring response to therapy.  

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