The gene mutation that identifies the lung cancer patients most likely to respond to the drug gefitinib (Iressa) is not associated with a response to the drug cetuximab (Erbitux), according to a new study published in the August 17 issue of the Journal of the National Cancer Institute. Both drugs target the same gene but through different mechanisms.
Some patients with non–small-cell lung cancer (NSCLC) have mutant versions of the epidermal growth factor receptor (EGFR). This protein activates signaling pathways involved with cell growth and survival. Previous studies have shown that small-molecule EGFR inhibitors such as gefitinib and erlotinib (Tarceva) work by blocking signals in the intracellular domain of EGFR--between the EGFR and the cell nucleus. Additionally, many NSCLC patients with mutations in this intracellular domain of EGFR appear to benefit from these drugs.
Toru Mukohara, M.D., of the Dana-Farber Cancer Institute in Boston, and colleagues decided to examine the effectiveness of another type of drug that targets EGFR--a monoclonal antibody called cetuximab, which is approved for the treatment of metastatic colorectal cancers that overexpress EGFR. Cetuximab targets EGFR by preventing its activation by extracellular signals, or signals occurring outside of the cell, as opposed to the intra-cellular signal blocking of drugs like gefitinib.
Elana Hayasaka | EurekAlert!
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