The DOI matches its Crossref record; 3 of the 3 references it cites were found in a registry or an index.
Functional ABCG2 is overexpressed on primary CML CD34+ cells and is inhibited by imatinib mesylate
Abstract
Imatinib mesylate (IM) therapy for chronic myeloid leukemia (CML) has transformed the treatment of this disease. However, the vast majority of patients, despite major responses, still harbor Philadelphia chromosome–positive (Ph+) cells. We have described a population of primitive Ph+ cells that are insensitive to IM and may be a source of IM resistance. Cell line studies have suggested that the drug transporter ABCG2 may be a mediator of IM resistance, however there is considerable debate about whether IM is an ABCG2 substrate or inhibitor. We demonstrate here that primitive CML CD34+ cells aberrantly overexpress functional ABCG2 but that cotreatment with IM and an ABCG2 inhibitor does not potentiate the effect of IM. We definitively show that IM is an inhibitor of, but not a substrate for, ABCG2 and that, therefore, ABCG2 does not modulate intracellular concentrations of IM in this clinically relevant cell population.
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Citations
Cites
Multidrug resistance in cancer: role of ATP–dependent transporters
Gottesman, M. M., Fojo, T., & Bates, S. E. (2002) · Nature Reviews Cancer · doi:10.1038/nrc706 · Cited by 5,536
Zhou, S., Schuetz, J. D., Bunting, K. D., Colapietro, A.-M., Sampath, J., Morris, J. J., Lagutina, I., Grosveld, G. C., Osawa, M., Nakauchi, H., et al. (2001) · Nature Medicine · doi:10.1038/nm0901-1028 · Cited by 2,280
Copland, M., Hamilton, A., Elrick, L. J., Baird, J. W., Allan, E. K., Jordanides, N., Barow, M., Mountford, J. C., & Holyoake, T. L. (2006) · Blood · doi:10.1182/blood-2005-07-2947 · Cited by 635
Self-citation
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
Chronic myeloid leukemia stem cells are not dependent on Bcr-Abl kinase activity for their survival
Hamilton, A., Helgason, G. V., Schemionek, M., Zhang, B., Myssina, S., Allan, E. K., Nicolini, F. E., Müller-Tidow, C., Bhatia, R., Brunton, V. G., et al. (2012) · Blood · doi:10.1182/blood-2010-12-326843 · Cited by 435
Self-citationLiu, W., Baer, M. R., Bowman, M. J., Pera, P., Zheng, X., Morgan, J., Pandey, R. A., & Oseroff, A. R. (2007) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-06-1599 · Cited by 136
Metadata
- Authors
- Jordanides, N. E., Jorgensen, H. G., Holyoake, T. L., & Mountford, J. C.
- Venue
- Blood
- Publisher
- American Society of Hematology
- Published
- 2006-08-15
- Volume
- 108
- Issue
- 4
- Pages
- 1370-1373
- ISSN
- 0006-4971 (ISSN-L)
- 1528-0020
- OpenAlex
- W2082469361
- Cited by
- 158
- References
- 3
- FWCI
- 8.37
- Type
- journal article
- Language
- en
- Open access
- closed
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- Jordanides, N. E., Jorgensen, H. G., Holyoake, T. L., & Mountford, J. C. (2006). Functional ABCG2 is overexpressed on primary CML CD34+ cells and is inhibited by imatinib mesylate. Blood. https://doi.org/10.1182/blood-2006-02-003145
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