The authors are at the Medical Oncology Research Program, Vall d'Hebron Research Institute and Vall d'Hebron University Hospital, Psg. Vall d'Hebron 119−129, Barcelona 08035, Spain. jbaselga@vhebron.net
When the tyrosine kinase inhibitor imatinib (Gleevec) was found to induce high remission rates in patients with chronic myeloid leukemia, this was hailed as a success for targeted tumor therapy. Since then, the repertoire of cancer types that respond to such inhibitors has expanded and researchers are beginning to grapple with the problem of acquired drug resistance. The activating kinase mutations targeted by these drugs can be viewed as the Achilles heel of cancer—they promote malignant progression, yet can turn cancer into a therapeutically exploitable disease.
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