Molecular Cytogenetic Study In Chronic Myeloid Leukaemia Treated With Imatinib

Background: Chronic myeloid leukaemia (CML) is a malignant myeloproliferative disorder of self-renewing haematopoietic stem cells. The top incidence occurs at the age of 45-55 years old and half of the patients are over 60 years old.CML is caused by a reciprocal chromosome translocation between chromosome 9 and 22, resulting in the short Philadelphia (Ph) chromosome carrying the BCR-ABL (Breakpoint Cluster Region-Abelson Leukaemia) oncogene. This oncogene encodes the chimeric BCR-ABL protein, which incorporates an activated ABL tyrosine kinase and is responsible for the initial chronic phase of CML. This phase of the disease is characterised by a massive expansion of granulocyte/macrophage progenitor cells. Acquisition of subsequent genetic abnormity then causes progression from the chronic phase to the terminal blast phase of the disease, characterised by an accumulation of either myeloid or lymphoid blast cells.CML can be treated in different ways, including conventional chemotherapeutics, interferon-α (IFN-α), allogenetic bone marrow transplantation and haematopoietic stem cell transplantation. In recent years, a breakthrough of the treatment of CML comes out with a novel compound, imaitnib. Imatinib mesylate (imaitnib, STI571, Glivec?/Gleevec?) is an ABL-specific tyrosine kinase inhibitor, which competitively binds to the ATP binding site of the BCR-ABL protein. The drug has shown outstanding effect and well tolerated. Now it has become the first-line therapy for this malignancy. In...