SUMMARY. Chronic myelogenous leukemia (CML) is a myelo-proliferative neoplasm arising from the appearance of abnormal hematopoietic stem cells that carry the Bcr-Abl oncoprotein, which results from a reciprocal translocation between chromosomes 9 and 22. The main elements of the disease pathogenesis are due to both increased tyrosine kinase activity of the Abl protein and the role of the Bcr part of the hybrid protein. The presence of the PH domain in Bcr determines its interaction with PI(3)P on the phagosomal membrane. We have shown that this interaction is accompanied by colocalization with the FNBPI protein in the phagosomes of J774 macrophage cells. A model of the impact of the Bcr-Abl oncoprotein on the ROS excess formation in CML due to the uncontrolled expression of phagosomal NADPH oxidase is presented.
Keywords: chronic myelogenous leukemia (CML), Bcr-Abl, FNBP1, phagosome, NADPH oxidase
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