Clinical Trial: Chromosome Abnormalities in Chronic Myeloid Leukemia (CML) on Imatinib. GIST Patients on Imatinib

Study Status: Terminated
Recruit Status: Terminated
Study Type: Interventional

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

Brief Summary: 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.

Detailed Summary:

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.

Sponsor: University Health Network, Toronto

Current Primary Outcome: ~ presence or absence of genetic abnormality as seen in CML patients on imatinib

Original Primary Outcome: Same as current

Current Secondary Outcome:

Original Secondary Outcome:

Information By: University Health Network, Toronto

Dates:
Date Received: April 16, 2007
Date Started: February 2005
Date Completion:
Last Updated: February 12, 2009
Last Verified: April 2007