Two Designer Drugs Hit Same Lung Cancer Target, But Only One Is Effective

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Treatment Drug - Lung Cancer

Study demonstrates presence or absence of gene mutation a critical factor in treatment choice

Two designer cancer drugs differed dramatically in a laboratory test comparing their ability to shut down a mutant, overactive growth signal in lung cancer cells, reports a team headed by scientists at the Dana-Farber Cancer Institute.

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Although both drugs killed cells containing a normal but overactive EGFR (epidermal growth factor receptor) molecule, only gefitinib (Iressa) killed lung cancer cells containing a mutated EGFR molecule. The monoclonal antibody drug cetuximab (Erbitux) had little effect on the mutant signal, evidently because it strikes at a different part of the EGFR molecule.

Reporting in the Aug. 17 issue of the Journal of the National Cancer Institute, the researchers say that the divergent results add to growing evidence that mutations in the targets of designer drugs critically influence their effectiveness. Erbitux is an effective inhibitor of EGFR signals in colorectal cancer, which involves a normal, not mutant, EGFR molecule.

"We now know of several groups of patients who benefit from therapy targeted at EGFR," says Pasi A. J

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