The DOI matches its Crossref record; 32 of the 32 references it cites were found in a registry or an index.
Mechanism of resistance to the ABL tyrosine kinase inhibitor STI571 in BCR/ABL–transformed hematopoietic cell lines
Abstract
The tyrosine kinase activity of the Bcr/Abl oncogene is required for transformation of hematopoietic cells. The tyrosine kinase inhibitor STI571 (formerly called CGP57148B, Novartis Pharmaceuticals) inhibits BCR/ABL, TEL/ABL, and v-ABL kinase activity and inhibits growth and viability of cells transformed by any of these ABL oncogenes. Here we report the generation of 2 BCR/ABL–positive cell lines that have developed partial resistance to STI571. BCR/ABL–transformed Ba/F3 hematopoietic cells and Philadelphia-positive human K562 cells were cultured in gradually increasing concentrations of STI571 over a period of several months to generate resistant lines. Resistant Ba/F3.p210 cells were found to have an increase in Bcr/Abl messenger RNA, amplification of the Bcr/Abl transgene, and a greater than tenfold increase in the level of BCR/ABL protein. In contrast to Ba/F3.p210 cells, drug-resistant K562 cells did not undergo detectable amplification of the BCR/ABL gene, although they displayed a 2-fold to 3-fold increase in p210BCR/ABL protein. The addition of STI571 to both resistant Ba/F3.p210 and K562 cells resulted in a rapid reduction of tyrosine phosphorylation of cellular proteins, similar to that observed for nonresistant cells. However, the inhibition of kinase activity was transient and partial and was not accompanied by apoptosis. The results suggest that resistance to STI571 may be multifactorial. Increased expression of the target protein BCR/ABL was observed in both lines, and resulted from oncogene amplification in one line. However, altered drug metabolism, transport, or other related mechanisms may also contribute to drug resistance.
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Citations
Cites
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The tyrosine kinase inhibitor CGP57148B selectively inhibits the growth of BCR-ABL-positive cells
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Cited by
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
Druker, B. J., Sawyers, C. L., Kantarjian, H., Resta, D. J., Reese, S. F., Ford, J. M., Capdeville, R., & Talpaz, M. (2001) · New England Journal of Medicine · doi:10.1056/nejm200104053441402 · Cited by 2,713
The development of imatinib as a therapeutic agent for chronic myeloid leukemia
Deininger, M., Buchdunger, E., & Druker, B. J. (2005) · Blood · doi:10.1182/blood-2004-08-3097 · Cited by 1,253
Talpaz, M. (2002) · Blood · doi:10.1182/blood.v99.6.1928 · Cited by 1,019
Branford, S., Rudzki, Z., Walsh, S., Grigg, A., Arthur, C., Taylor, K., Herrmann, R., Lynch, K. P., & Hughes, T. P. (2002) · Blood · doi:10.1182/blood.v99.9.3472 · Cited by 649
Metadata
- Authors
- Weisberg, E., & Griffin, J. D.
- Venue
- Blood
- Publisher
- American Society of Hematology
- Published
- 2000-06-01
- Volume
- 95
- Issue
- 11
- Pages
- 3498-3505
- ISSN
- 0006-4971 (ISSN-L)
- 1528-0020
- OpenAlex
- W2263837564
- Cited by
- 401
- References
- 32
- FWCI
- 30.01
- Type
- journal article
- Language
- en
- Open access
- closed
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- Weisberg, E., & Griffin, J. D. (2000). Mechanism of resistance to the ABL tyrosine kinase inhibitor STI571 in BCR/ABL–transformed hematopoietic cell lines. Blood. https://doi.org/10.1182/blood.v95.11.3498
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