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News and Views
Nature Medicine 12, 1125 - 1126 (2006)
doi:10.1038/nm1006-1125
Targeted cancer treatment: resisting arrest
Dominik Wodarz1
- Dominik Wodarz is in the Department of Ecology and Evolutionary Biology, 321 Steinhaus Hall, University of California, Irvine, California 92697, USA. e-mail: dwodarz@uci.edu
Abstract
Many individuals with chronic myeloid leukemia have benefited from the drug imatinib (Gleevec)—but if they are taken off the drug, relapse occurs. Two mathematical models to explain this phenomenon, one described in this issue, have come to different conclusions (1181–1184).
Knowledge of molecular pathways responsible for carcinogenesis has allowed the development of targeted therapies that specifically attack abnormalities in cancer cells1. The treatment of chronic myeloid leukemia (CML) with imatinib (Gleevec) has benefited patients in this context2, but problems remain.
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