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Several Bcr-Abl kinase domain mutants associated with imatinib mesylate resistance remain sensitive to imatinib
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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“As reported previously (Corbin et al., 2003), addition of up to 3 mM Imatinib alone had little effect on proliferation of these cells (less than 10% inhibition, Figure 5D).”
From Rac Guanosine Triphosphatases Represent Integrating Molecular Therapeutic Targets for BCR-ABL-Induced Myeloproliferative Disease (2007) · cites this paper as Corbin et al., 2003
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Cites
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Cited by
O'Hare, T., Walters, D. K., Stoffregen, E. P., Jia, T., Manley, P. W., Mestan, J., Cowan-Jacob, S. W., Lee, F. Y., Heinrich, M. C., Deininger, M. W. N., et al. (2005) · Cancer Research · doi:10.1158/0008-5472.can-05-0259 · Cited by 1,036
Self-citationBradeen, H. A., Eide, C. A., O'Hare, T., Johnson, K. J., Willis, S. G., Lee, F. Y., Druker, B. J., & Deininger, M. W. (2006) · Blood · doi:10.1182/blood-2006-02-004580 · Cited by 393
Self-citationThomas, E. K., Cancelas, J. A., Chae, H.-D., Cox, A. D., Keller, P. J., Perrotti, D., Neviani, P., Druker, B. J., Setchell, K. D. R., Zheng, Y., et al. (2007) · Cancer Cell · doi:10.1016/j.ccr.2007.10.015 · Cited by 147
Self-citationJabbour, E. J., Cortes, J. E., & Kantarjian, H. M. (2013) · Clinical Lymphoma Myeloma and Leukemia · doi:10.1016/j.clml.2013.03.018 · Cited by 105
Chronic Myeloid Leukemia: Mechanisms of Resistance and Treatment
Jabbour, E., Parikh, S. A., Kantarjian, H., & Cortes, J. (2011) · Hematology/Oncology Clinics of North America · doi:10.1016/j.hoc.2011.09.004 · Cited by 68
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
- Cited by
- 258
- References
- 1
- Language
- en
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- CoChat. (2026). Citation check: Several Bcr-Abl kinase domain mutants associated with imatinib mesylate resistance remain sensitive to imatinib. https://app.cochat.ai/papers/10.1182/blood-2002-12-3659
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- Corbin, A. S., Rosée, P. L., Stoffregen, E. P., Druker, B. J., & Deininger, M. W. (2003). Several Bcr-Abl kinase domain mutants associated with imatinib mesylate resistance remain sensitive to imatinib. Blood. https://doi.org/10.1182/blood-2002-12-3659
