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

This study has been terminated.
(study terminated 12Feb09 due to low recruitment)
Sponsor:
Collaborators:
Princess Margaret Hospital, Canada
Mount Sinai Hospital, Canada
Novartis
Information provided by:
University Health Network, Toronto
ClinicalTrials.gov Identifier:
NCT00461929
First received: April 16, 2007
Last updated: February 12, 2009
Last verified: April 2007

April 16, 2007
February 12, 2009
February 2005
December 2008   (final data collection date for primary outcome measure)
~ presence or absence of genetic abnormality as seen in CML patients on imatinib
Same as current
Complete list of historical versions of study NCT00461929 on ClinicalTrials.gov Archive Site
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Chromosome Abnormalities in Chronic Myeloid Leukemia (CML) on Imatinib. GIST Patients on Imatinib
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.

Interventional
Phase 4
Allocation: Non-Randomized
Intervention Model: Single Group Assignment
Masking: Open Label
Primary Purpose: Diagnostic
  • Chronic Myeloid Leukemia
  • Gastrointestinal Stromal Cell Tumors
  • Chromosome Abnormality
Procedure: bone marrow aspiration
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*   Includes publications given by the data provider as well as publications identified by ClinicalTrials.gov Identifier (NCT Number) in Medline.
 
Terminated
68
December 2008
December 2008   (final data collection date for primary outcome measure)

Inclusion Criteria:

  • GIST patient on Imatinib for more than 12 months

Exclusion Criteria:

  • nil
Both
18 Years and older
No
Contact information is only displayed when the study is recruiting subjects
Canada
 
NCT00461929
CST1571ACA10 GIST
No
Dr. Jeff Lipton, University Health Network, Princess Margaret Hospital
University Health Network, Toronto
  • Princess Margaret Hospital, Canada
  • Mount Sinai Hospital, Canada
  • Novartis
Principal Investigator: Jeff Lipton, MD University Health Network, DMOH
Study Director: Martin Blackstein, MD Mount Sinai Hospital, New York
University Health Network, Toronto
April 2007

ICMJE     Data element required by the International Committee of Medical Journal Editors and the World Health Organization ICTRP