Chronic Myeloid Leukemia Clinical Trial
Official title:
Are the Secondary Chromosome Abnormalities Seen in Chronic Myeloid Leukemia (CML) Cells Induced to Ph-Chromosome Negativity by Imatinib a Result of Chromosome Instability or a Side Effect of the Therapy - a Study in GIST (Gastrointestinal Stromal Cell Tumors) Patients Treated With Imatinib.
In order to distinguish between clonal instability driven by imatinib in CML and actual changes with secondary clones induced by imatinib we would like to investigate the karyotype of non-CML patients treated with imatinib such as GIST patients.
Chronic myeloid leukemia (CML) is a myeloproliferative disorder characterized by the
presence of the Philadelphia (Ph) chromosome - a t(9:22) translocation that results in the
production of a BCR/ABL fusion protein with Abl kinase activity.
Imatinib mesylate (Gleevec) specifically targets a limited set of protein tyrosine kinases -
ABL, Arg (Abl-related gene), c-Kit, platelet-derived growth factor receptor (PDGF-R) - and
their oncogenic forms, most notably BCR/ABL Imatinib is also a potent inhibitor of a
receptor-type c-Kit tyrosine kinase. Therefore imatinib was examined for therapeutic
efficacy against malignant gastro-intestinal stromal tumors (GIST) Recent articles have
drawn attention to the development of new Ph-negative, cytogenetically unrelated clones
after therapy of Ph-positive CML with imatinib. Trisomy 8 and monosomy 7 are the most
frequent defects, but other aberrations have also been reported. Some of these cytogenetic
abnormalities are associated with acute myeloid leukemia and MDS.
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Allocation: Non-Randomized, Intervention Model: Single Group Assignment, Masking: Open Label, Primary Purpose: Diagnostic
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