Findings shed light on how gefitinib fights lung cancer
Gefitinib destroys lung cancer cells, in part, by inhibiting survival signals transduced by mutant epidermal growth factor receptors (EGFRs), the findings of new study suggest.
Gefitinib has been shown to be an effective treatment for non-small cell lung cancers (NSCLCs), but only cancers with activating mutations in EGFR typically respond to the drug. However, the signaling effects of these mutant EGFRs are unclear. In a study reported in the July 29th online issue of Science, Dr. Jeffrey Settleman, from Harvard Medical School in Boston, and colleagues evaluated the signaling effects of mutant EGFRs. The mutant EGFRs activated certain signaling pathways, known as Akt and STAT, which promoted survival of the cancer cell, the authors note. By contrast, the mutants had no effect on cell proliferation mediated by Erk/MAPK signaling. In NSCLCs harboring mutant EGFRs, experimentally removing the mutant or blocking Akt/STAT signaling produced extensive apoptosis. Cells treated in either fashion were relatively resistant to conventional chemotherapeutic agents, the researchers note.The results indicate that “mutant EGFRs selectively transduce survival signals on which NSCLCs become dependent; inhibition of those signals by gefitinib may contribute to the drug’s efficacy,” the authors conclude. (Source: Science: Reuters Health News: Oncolink: August 2004.)
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