New Orleans—The goal of most cancer research
is to better understand how a cell becomes malignant and how to use that information
to help successfully treat patients in an individualized manner. Therapies
that zero in on specific targets—such as a particular enzyme or a receptor
on the surface of a cell—may be able to assault a patient's cancer cells
while steering clear of normal cells.
This has been the rationale for the development of anticancer drugs
such as imatinib and gefitinib. These drugs have been shown to be effective
for subsets of patients who have malignancies associated with abnormal versions
of the tyrosine kinases KIT and epidermal growth factor receptor (EGFR), respectively.
(Kinases are enzymes important for transmitting signals within cells; many
play roles in cell differentiation and division.) Researchers have identified
specific genetic alterations in the genes that encode KIT and EGFR that explain
why the therapies work well for some patients but provide little or no benefit
Hampton T. "Promiscuous" Anticancer Drugs That Hit Multiple Targets May Thwart Resistance. JAMA. 2004;292(4):419-422. doi:10.1001/jama.292.4.419