Researchers at Memorial Sloan-Kettering Cancer Center (MSKCC) have found an explanation for why some lung cancers stop responding to the drugs erlotinib (TarcevaTM) and gefitinib (Iressa®). This discovery may lead to the development of new therapies to use when these agents stop working. The research is to be published online in the open-access international journal PLoS Medicine on February 22, 2005.*
Gefitinib and erlotinib are so-called targeted therapies, in that they halt the growth of certain cancers by zeroing in on a signaling molecule critical to the survival of those cancer cells. The two drugs are effective in about 10 percent of US patients with non-small cell lung cancer (NSCLC). Previous work from this group at MSKCC and from groups at Harvard Medical School showed that the two drugs work specifically in patients whose cancers contain mutations in a gene that encodes the epidermal growth factor receptor (EGFR). The MSKCC team has also shown that lung cancer patients with these mutations are often people who have never smoked.
"Although these targeted therapies are initially effective in this subset of patients, the drugs eventually stop working, and the tumors begin to grow again. We call this acquired or secondary resistance," said Vincent A. Miller, MD, a thoracic oncologist at MSKCC and one of the study’s two lead authors. "This is different from primary resistance, which means that the drugs never work at all," Dr. Miller said.
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