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Chronic myeloid leukemia and the Fas-FasL system

With therapeutic advances that include imatinib mesylate, bone marrow transplantation and donor lymphocyte infusion, life expectancy of chronic myeloid leukemia carriers has increased significantly and the disease might not be fatal. However, the biological mechanisms that favor the selection of malignant clone cells over normal cells, in most cases responsible for the lack of therapeutic success, are still unclear. Alterations in cellular apoptosis process and escape of the leukemic cells from the anti-tumor immune response can explain, in part, the selective advantages of these cells. The apoptosis process or programmed cell death can be triggered by intrinsic or extrinsic pathways. The extrinsic is dependent on the interaction of cell death receptors, such as the Fas receptor and its agonist, the Fas ligand (FasL). A diminished expression of Fas and increased of FasL in leukemic cell may increase its survival, thereby making it resistant to apoptosis. This paper describes the relation between chronic myeloid leukemia and the Fas/FasL system and its possible importance in prognosis and in escape of the leukemic cells from the immune system.

Chronic myeloid leukemia; Fas/FasL system; apoptosis


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