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Several Bcr-Abl kinase domain mutants associated with imatinib mesylate resistance remain sensitive to imatinib

Corbin, Amie S., Rosée, Paul La, Stoffregen, Eric P., Druker, Brian J., Deininger, Michael W.·2003·Blood
DOI 10.1182/blood-2002-12-3659
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Abstract

Imatinib mesylate is a selective Bcr-Abl kinase inhibitor, effective in the treatment of chronic myelogenous leukemia. Most patients in chronic phase maintain durable responses; however, many in blast crisis fail to respond, or relapse quickly. Kinase domain mutations are the most commonly identified mechanism associated with relapse. Many of these mutations decrease the sensitivity of the Abl kinase to imatinib, thus accounting for resistance to imatinib. The role of other mutations in the emergence of resistance has not been established. Using biochemical and cellular assays, we analyzed the sensitivity of several mutants (Met244Val, Phe311Leu, Phe317Leu, Glu355Gly, Phe359Val, Val379Ile, Leu387Met, and His396Pro/Arg) to imatinib mesylate to better understand their role in mediating resistance.While some Abl mutations lead to imatinib resistance, many others are significantly, and some fully, inhibited. This study highlights the need for biochemical and biologic characterization, before a resistant phenotype can be ascribed to a mutant.

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Crossref · 10.1182/blood-2002-12-3659

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Citations

Cites

Research works printed but not linked: 22

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Metadata

Authors
Corbin, A. S., Rosée, P. L., Stoffregen, E. P., Druker, B. J., & Deininger, M. W.
Affiliations
From the Oregon Health and Science University Cancer Institute, Division of Hematology and Medical Oncology, Portland, OR; and III Medizinische Universitätsklinik, Fakultät für klinische Medizin Mannheim der Universität Heidelberg, Mannheim, Germany.
Venue
Blood
Publisher
American Society of Hematology
Published
2003-06-01
Volume
101
Issue
11
Pages
4611-4614
ISSN
  • 0006-4971
  • 1528-0020
DOI
10.1182/blood-2002-12-3659
Cited by
258
References
1
Language
en

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