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Inhibition of Mutant EGF Receptors by Gefitinib: Targeting an Achilles’ Heel of Lung Cancer
Jeffrey Settleman
volume 3 | issue 12
december 2004Pages: 1496 - 1497
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Recent reports revealed a strong correlation between the presence of somatic activating mutations in the kinase domain of the EGF receptor in some human lung cancers and a striking clinical response to the selective EGF receptor inhibitor, Gefitinib. These oncogenic receptors exhibit altered signaling properties such that they selectively activate downstream survival pathways on which tumor cells have become dependent. Thus, tumor cells are effectively killed by Gefitinib treatment. In addition, the catalytic function of the mutant receptors exhibits increased sensitivity to Gefitinib, raising the possibility that two distinct consequences of Gefitinib action account for its clinical efficacy.
We now provide open access to journal articles published online for one year or more. This article may be downloaded at the following link:
Download PDF If the document does not open, please right-click on the link (control-click on a Macintosh) and select the option to save the file to disk.