Chronic Myeloid Leukemia (CML) is a clonal disorder of the hematopoietic stem cell caused by the BCR-ABL receptor tyrosinekinase. The hallmark of CML is Philadelphia (Ph) chromosome. The Philadelphia chromosome (Ph) is a shortened of chromosome 22 which is due to reciprocal translocation of chromosome 9 and 22. This translocation leads to formation of the BCR-ABL fusion oncogene gene, the protein product of which (p210, p190 and rarely p230) has constitutive tyrosine kinase activity implicated in the pathogenesis of the disease. Chronic Myelogenous Leukemia (CML) has a typical progressive course with transition from the chronic phase to the terminal blast crisis phase. The mechanisms that lead to disease progression have yet to be elucidated.
Inactivation of P16 (INK4a) Gene by Promoter Hypermethylation is Associated with Disease Progression in Chronic Myelogenous Leukaemia
Last date updated on December, 2020