The DOI matches its Crossref record; 32 of the 32 references it cites were found in a registry or an index.
MDR1 gene overexpression confers resistance to imatinib mesylate in leukemia cell line models
Open accessAbstract
Inappropriate expression of the multidrug resistance(MDR1) gene encoding the P-glycoprotein (Pgp) has been frequently implicated in resistance to different chemotherapeutic drugs. We have previously generated chronic myeloid leukemia (CML) cell lines resistant to the tyrosine kinase inhibitor imatinib mesylate (STI571), and one line (LAMA84-r) showed overexpression not only of the Bcr-Abl protein but also of Pgp. In the present study, we investigated this phenomenon in other cell lines overexpressing exclusively Pgp. Thus, cells from the K562/DOX line, described as resistant to doxorubicin due to MDR1 gene overexpression, grew continuously in the presence of 1 μM imatinib, but died in 4 to 5 days if the Pgp pump modulators verapamil or PSC833 were added to the imatinib-treated culture. Analysis of cell proliferation by the MTS (3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium) assay confirmed the differential sensitivity of K562/DOX to imatinib, which was also reversed by verapamil or PSC833. Flow cytometric analysis of the total phosphotyrosine content by intracytoplasmic staining after a 2-hour incubation with escalating doses of imatinib showed that the inhibitory concentrations of 50% (IC50) for inhibition of cellular protein tyrosine phosphorylation were 15, 10, and 5 μM for K562/DOX, K562/DOX plus verapamil, and K562, respectively. Retroviral-mediated transfection of theBCR-ABL+ AR230 cell line with theMDR1 gene decreased its sensitivity to imatinib, an effect that was also reversed by verapamil. The possible role of MDR overexpression in clinical resistance to imatinib remains to be defined. We therefore confirm that imatinib should be added to the extensive list of drugs that can be affected by the MDR phenomenon.
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Effects of a selective inhibitor of the Abl tyrosine kinase on the growth of Bcr-Abl positive cells
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Cited by
Corbin, A. S., Agarwal, A., Loriaux, M., Cortes, J., Deininger, M. W., & Druker, B. J. (2011) · Journal of Clinical Investigation · doi:10.1172/jci35721 · Cited by 765
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Strategies to overcome resistance to targeted protein kinase inhibitors
Daub, H., Specht, K., & Ullrich, A. (2004) · Nature Reviews Drug Discovery · doi:10.1038/nrd1579 · Cited by 334
Lei, H., Xu, H.-Z., Shan, H.-Z., Liu, M., Lu, Y., Fang, Z.-X., Jin, J., Jing, B., Xiao, X.-H., Gao, S.-M., et al. (2021) · Nature Communications · doi:10.1038/s41467-020-20259-0 · Cited by 146
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Metadata
- Authors
- Mahon, F.-X., Belloc, F., Lagarde, V., Chollet, C., Moreau-Gaudry, F., Reiffers, J., Goldman, J. M., & Melo, J. V.
- Venue
- Blood
- Publisher
- American Society of Hematology
- Published
- 2003-03-15
- Volume
- 101
- Issue
- 6
- Pages
- 2368-2373
- ISSN
- 0006-4971 (ISSN-L)
- 1528-0020
- OpenAlex
- W2098785293
- Cited by
- 538
- References
- 32
- FWCI
- 16.05
- Type
- journal article
- Language
- en
- Open access
- bronze
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- Mahon, F.-X., Belloc, F., Lagarde, V., Chollet, C., Moreau-Gaudry, F., Reiffers, J., Goldman, J. M., & Melo, J. V. (2003). MDR1 gene overexpression confers resistance to imatinib mesylate in leukemia cell line models. Blood. https://doi.org/10.1182/blood.v101.6.2368
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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