>In an accompanying editorial, Brian Druker, M.D., of the Oregon Health and Science University Cancer Institute in Portland, points out that the concentrations of imatinib required to inhibit cell proliferation and to block c-kit activation suggest that c-kit is not the primary target of imatinib and that such high concentrations may not be achievable in the clinical setting.

The promise, he concludes, is that identification of another imatinib-sensitive kinase in Ewing's sarcoma cells could lead to improved therapy for this disease.

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Contact: Linda Wang
jncimedia@oupjournals.org
301-841-1287
Journal of the National Cancer Institute
19-Nov-2002

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