Myeloid Leukaemia (CML) is a clonal disorder of a pluripotent stem cell
characterized by the Philadelphia (Ph) chromosome. The Ph is a shortened
chromosome 22 resulting from a reciprocal translocation between the BCR gene on chromosome 22 and the ABL gene on chromosome 9 (Mondal et
al., 2006). The resulting overactive ABL tyrosine kinase appears to be
responsible for uncontrolled myeloid cell proliferation (Hughes et al., 2006).
Imatinib, also called Gliveec, is the first and most commonly used tyrosine
kinase inhibitor (TKI) that inhibits by binding through ATP (adenosine
triphosphate) onto the BCR-ABL fusion
protein of which when absent the kinase leads to uncontrolled cell
proliferation. The level of BCR-ABL mRNA
can be used as a sensitive marker for disease progression (Hoffbrand et al.,
2001). In approximately 5% of CML cases, patients present with a variant Ph
chromosome in which the Ph chromosome is derived through rearrangements other
than the classic t(9;22) (Hughes, et al., 2006).
aim of this study is to assess the response to therapy between classic chronic
myeloid leukaemia patients and variant translocation chronic myeloid leukaemia
patients. Methods for monitoring treatment response include conventional
cytogenetic analysis, Fluorescence in situ hybridization (FISH) and
Quantitative PCR (polymerase chain reaction). BCR-ABL transcript levels quantified by PCR will be used to
assess the response of therapy, which in turn influences the choice of clinical
management. The response in therapy will be monitored in patients with variant
Ph translocations compared to patients with classical Ph translocation who have
or have not responded to treatment.
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