It emerged a seductive idea: Bridging the gap between genetics and pharmacology could allow clinicians to hit cancer cells where it hurts them most. In May 2004, Iressa, known generically as gefitinib, rose from the ashes of poor clinical trials as an example of how this might work. But this early poster child for pharmacogenetics has yet to live up to its hype.
A tyrosine kinase inhibitor, Iressa blocks the epidermal growth factor receptor (EGFR), a protein overexpressed in many tumors. Results of clinical trials were disappointing in 2003, as most patients with non-small-cell lung cancer did not benefit from the drug. Roughly 10% of patients, many of them Japanese, considerably improved, however, as their tumors seemed to melt away. "The results were puzzling," says Matthew Meyerson of the Dana-Farber Cancer Institute in Boston. Everyone wanted to know: What was different about this 10%?
In the three Hot Papers featured ...
