Abstract
Chronic myeloid leukemia (CML) is a clonal hematopoietic stem cell disorder. The cytogenetic hallmark of CML is the Philadelphia (Ph) chromosome, which is a shortened chromosome 22 that results from a reciprocal translocation between the long arms of chromosomes 9 and 22. The molecular consequence of this translocation is the fusion of the c-abl oncogene from chromosome 9 with sequences from chromosome 22, the breakpoint cluster region (BCR), giving rise to a fused BCR-ABL gene. Imatinib mesylate is a potent inhibitor for ABL tyrosine kinases, including BCRABL. It induces cytogenetic and/or hematologic response, improving survival in patients with CML. It has also been shown to inhibit c-KIT and the platelet-derived growth factor receptor tyrosine kinases. The c-KIT, a transmembrane tyrosine kinase, binds the stem-cell factor and is believed to be essential for the development and maintenance of normal haematopoiesis, mast cells, melanocytes, germ cells, and interstitial cells of Cajal. Gastrointestinal stromal tumors (GIST) are the most common mesenchymal neoplasms of the gastrointestinal tract, which express the c-KIT proto-oncogene [1]. Imatinib mesylate targets the surface tyrosine kinase receptor KIT .I t is approved for treatment of patients with KIT-positive unresectable and/or metastatic malignant GIST (Table 1). Here, we report two cases of CML accompanied by GIST. The coincidence of these neoplasms is extremely rare demographically.
Published Version
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