| Literature DB >> 16645167 |
Els Lierman1, Cedric Folens, Elizabeth H Stover, Nicole Mentens, Helen Van Miegroet, Werner Scheers, Marc Boogaerts, Peter Vandenberghe, Peter Marynen, Jan Cools.
Abstract
The FIP1L1-PDGFRA oncogene is a common cause of chronic eosinophilic leukemia (CEL), and encodes an activated tyrosine kinase that is inhibited by imatinib. FIP1L1-PDGFRA-positive patients with CEL respond to low-dose imatinib therapy, but resistance due to acquired T674I mutation has been observed. We report here the identification of sorafenib as a potent inhibitor of the FIP1 like 1-platelet-derived growth factor receptor alpha (FIP1L1-PDGFRalpha) (T674I) mutant. Sorafenib inhibited the proliferation of FIP1L1-PDGFRalpha and FIP1L1-PDGFRalpha(T674I)-transformed Ba/F3 cells and induced apoptosis of the EOL-1 cell line at a low nanomolar concentration. Western blot analysis confirmed that these effects were due to a direct effect on FIP1L1-PDGFRalpha and FIP1L1-PDGFRalpha(T674I). Sorafenib was recently approved for the treatment of renal cell carcinoma. Our data suggest that low doses of sorafenib could be efficient for the treatment of FIP1L1-PDGFRA-positive CEL and could be used to overcome resistance to imatinib associated with the T674I mutation.Entities:
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Year: 2006 PMID: 16645167 PMCID: PMC1895882 DOI: 10.1182/blood-2006-02-004457
Source DB: PubMed Journal: Blood ISSN: 0006-4971 Impact factor: 22.113