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Inhibition of c-fms by imatinib: expanding the spectrum of treatment

Citation

Dewar, AL and Zannettino, ACW and Hughes, TP and Lyons, AB, Inhibition of c-fms by imatinib: expanding the spectrum of treatment, Cell Cycle, 4, (7) pp. 38-40. ISSN 1538-4101 (2005) [Refereed Article]

DOI: doi:10.4161/cc.4.7.1788

Abstract

Imatinib is a selective protein tyrosine kinase inhibitor currently used in the treatment of chronic myeloid leukaemia (CML). It specifically suppresses the growth of bcr-abl expressing CML progenitor cells by blocking the ATP-binding site of the kinase domain of bcr-abl. Imatinib also inhibits the c-abl, platelet derived growth factor receptor (PDGFR), abl-related gene and stem cell factor receptor, c-kit, protein tyrosine kinases. It is through inhibition of c-kit that imatinib is also used clinically in the treatment of gastrointestinal stromal tumours. We have recently demonstrated that imatinib also specifically targets the macrophage colony stimulating factor receptor, c-fms, at therapeutic concentrations. Although this finding has important implications with regard to potential side effects in patients currently receiving imatinib therapy, these results suggest that imatinib may also be useful in the treatment of diseases where c-fms is implicated. This includes breast and ovarian cancer and inflammatory conditions such as rheumatoid arthritis. We also speculate that imatinib may be used in diseases where bone destruction occurs due to excessive osteoclast activity, such as in the haematologic malignancy, multiple myeloma.

Item Details

Item Type:Refereed Article
Research Division:Medical and Health Sciences
Research Group:Immunology
Research Field:Cellular Immunology
Objective Division:Health
Objective Group:Clinical Health (Organs, Diseases and Abnormal Conditions)
Objective Field:Immune System and Allergy
Author:Lyons, AB (Dr Bruce Lyons)
ID Code:73622
Year Published:2005
Web of Science® Times Cited:38
Deposited By:Medicine (Discipline)
Deposited On:2011-10-19
Last Modified:2012-02-27
Downloads:0

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