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BCR-ABL point mutants isolated from patients with imatinib mesylate-resistant chronic myeloid leukemia remain sensitive to inhibitors of the BCR-ABL chaperone heat shock protein 90
Abstract
Clinical resistance to imatinib mesylate is commonly observed in patients with advanced Philadelphia chromosome– positive (Ph+) leukemias. Acquired resistance is typically associated with reactivation of BCR-ABL due to kinase domain mutations or gene amplification, indicating that BCR-ABL remains a viable target for inhibition in these patients. Strategies for overcoming resistance can be envisioned through exploitation of other molecular features of the BCR-ABL protein, such as its dependence on the molecular chaperone heat shock protein 90 (Hsp90). To determine whether inhibition of Hsp90 could induce degradation of imatinib mesylate–resistant, mutant BCR-ABL proteins, hematopoietic cells expressing 2 mutant BCR-ABL proteins found in imatinib mesylate–resistant patients (T315I and E255K) were examined for sensitivity to geldanamycin and 17-allylaminogeldanamycin (17-AAG). Both compounds induced the degradation of wild-type and mutant BCR-ABL and inhibited cell growth, with a trend indicating more potent activity against mutant BCR-ABL proteins. These data support clinical investigations of 17-AAG in imatinib mesylate–resistant Ph+ leukemias.
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“However, molecular remissions in response to Imatinib are not uniform and kinase domain mutations have been identified that are resistant to Imatinib therapy (Gorre et al., 2002;Lowenberg, 2003).”
From Rac Guanosine Triphosphatases Represent Integrating Molecular Therapeutic Targets for BCR-ABL-Induced Myeloproliferative Disease (2007) · cites this paper as Gorre et al., 2002
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Cites
Clinical Resistance to STI-571 Cancer Therapy Caused by BCR-ABL Gene Mutation or Amplification
Gorre, M. E., Mohammed, M., Ellwood, K., Hsu, N., Paquette, R., Rao, P. N., & Sawyers, C. L. (2001) · Science · doi:10.1126/science.1062538 · Cited by 3,104
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Research works printed but not linked: 24
- Sawyers, 1999, Chronic myeloid leukemia., N Engl J Med., 340, 1330, 10.1056/NEJM199904293401706 · DOI
- Faderl, 1999, The biology of chronic myeloid leukemia., N Engl J Med., 341, 164, 10.1056/NEJM199907153410306 · DOI
- Konopka, 1985, Cell lines and clinical isolates derived from Ph1-positive chronic myelogenous leukemia patients express c-abl proteins with a common structural alteration., Proc Natl Acad Sci U S A., 82, 1810, 10.1073/pnas.82.6.1810 · DOI · Paper page
- Daley, 1990, Induction of chronic myelogenous leukemia in mice by the P210bcr/abl gene of the Philadelphia chromosome., Science., 247, 824, 10.1126/science.2406902 · DOI · Paper page
- Heisterkamp, 1990, Acute leukaemia in bcr/abl transgenic mice., Nature., 344, 251, 10.1038/344251a0 · DOI
- Druker, 2001, Efficacy and safety of a specific inhibitor of the BCR-ABL tyrosine kinase in chronic myeloid leukemia., N Engl J Med., 344, 1031, 10.1056/NEJM200104053441401 · DOI
- Druker, 2001, Activity of a specific inhibitor of the BCR-ABL tyrosine kinase in the blast crisis of chronic myeloid leukemia and acute lymphoblastic leukemia with the Philadelphia chromosome., N Engl J Med., 344, 1038, 10.1056/NEJM200104053441402 · DOI · Paper page
- Branford, 2002, High frequency of point mutations clustered within the adenosine triphosphate-binding region of BCR/ABL in patients with chronic myeloid leukemia or Ph-positive acute lymphoblastic leukemia who develop imatinib (STI571) resistance., Blood., 99, 3472, 10.1182/blood.V99.9.3472 · DOI
- Hofmann, 2002, Ph(+) acute lymphoblastic leukemia resistant to the tyrosine kinase inhibitor STI571 has a unique BCR-ABL gene mutation., Blood., 99, 1860, 10.1182/blood.V99.5.1860 · DOI
- von Bubnoff, 2002, BCR-ABL gene mutations in relation to clinical resistance of Philadelphia-chromosome-positive leukaemia to STI571: a prospective study., Lancet., 359, 487, 10.1016/S0140-6736(02)07679-1 · DOI
- Shah, 2001, Resistance to Gleevec: sequence analysis reveals a spectrum of BCR/ABL kinase domain mutations in both acquired and de novo-resistant cases of CML in myeloid blast crisis. American Society of Hematology 43rd Annual Meeting.
- An, 2000, The heat shock protein 90 antagonist geldanamycin alters chaperone association with p210bcr-abl and v-src proteins before their degradation by the proteasome., Cell Growth Differ., 11, 355
- Shiotsu, 2000, Novel oxime derivatives of radicicol induce erythroid differentiation associated with preferential G(1) phase accumulation against chronic myelogenous leukemia cells through destabilization of Bcr-Abl with Hsp90 complex., Blood., 96, 2284, 10.1182/blood.V96.6.2284 · DOI
- Prodromou, 1997, Identification and structural characterization of the ATP/ADP-binding site in the Hsp90 molecular chaperone., Cell., 90, 65, 10.1016/S0092-8674(00)80314-1 · DOI
- Stebbins, 1997, Crystal structure of an Hsp90-geldanamycin complex: targeting of a protein chaperone by an antitumor agent., Cell., 89, 239, 10.1016/S0092-8674(00)80203-2 · DOI
- Grenert, 1997, The amino-terminal domain of heat shock protein 90 (hsp90) that binds geldanamycin is an ATP/ADP switch domain that regulates hsp90 conformation., J Biol Chem., 272, 23843, 10.1074/jbc.272.38.23843 · DOI
- Blagosklonny, 2001, The Hsp90 inhibitor geldanamycin selectively sensitizes Bcr-Abl-expressing leukemia cells to cytotoxic chemotherapy., Leukemia., 15, 1537, 10.1038/sj.leu.2402257 · DOI
- Nimmanapalli, 2001, Geldanamycin and its analogue 17-allylamino-17-demethoxygeldanamycin lowers Bcr-Abl levels and induces apoptosis and differentiation of Bcr-Abl-positive human leukemic blasts., Cancer Res., 61, 1799
- Muller, 1991, BCR first exon sequences specifically activate the BCR/ABL tyrosine kinase oncogene of Philadelphia chromosome-positive human leukemias., Mol Cell Biol., 11, 1785, 10.1128/MCB.11.4.1785 · DOI
- Goga, 1995, Alternative signals to RAS for hematopoietic transformation by the BCR-ABL oncogene., Cell., 82, 981, 10.1016/0092-8674(95)90277-5 · DOI
- Nichols, 1994, Identification of CRKL as the constitutively phosphorylated 39-kD tyrosine phosphoprotein in chronic myelogenous leukemia cells., Blood., 84, 2912, 10.1182/blood.V84.9.2912.2912 · DOI
- Oda, 1994, Crkl is the major tyrosine-phosphorylated protein in neutrophils from patients with chronic myelogenous leukemia., J Biol Chem., 269, 22925, 10.1016/S0021-9258(17)31596-X · DOI
- Senechal, 1996, The CRKL adaptor protein transforms fibroblasts and functions in transformation by the BCR-ABL oncogene., J Biol Chem., 271, 23255, 10.1074/jbc.271.38.23255 · DOI
- ten Hoeve, 1994, Tyrosine phosphorylation of CRKL in Philadelphia+ leukemia., Blood., 84, 1731, 10.1182/blood.V84.6.1731.1731 · DOI
Cited by
Lamb, J., Crawford, E. D., Peck, D., Modell, J. W., Blat, I. C., Wrobel, M. J., Lerner, J., Brunet, J.-P., Subramanian, A., Ross, K. N., et al. (2006) · Science · doi:10.1126/science.1132939 · Cited by 5,257
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Dual or multi-targeting inhibitors: The next generation anticancer agents
Raghavendra, N. M., Pingili, D., Kadasi, S., Mettu, A., & Prasad, S. V. U. M. (2018) · European Journal of Medicinal Chemistry · doi:10.1016/j.ejmech.2017.10.021 · Cited by 333
Metadata
- Authors
- Gorre, M. E., Ellwood-Yen, K., Chiosis, G., Rosen, N., & Sawyers, C. L.
- Affiliations
- From the Department of Medicine and Molecular Biology Institute, David Geffen School of Medicine at University of California, Los Angeles, CA; the Department of Medicine and Program in Cell Biology, Memorial Sloan-Kettering Cancer Center, New York, NY.
- Venue
- Blood
- Publisher
- American Society of Hematology
- Published
- 2002-10-15
- Volume
- 100
- Issue
- 8
- Pages
- 3041-3044
- ISSN
- 1528-0020
- 0006-4971
- Cited by
- 227
- References
- 1
- Language
- en
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