This Article  • Full text  • PDF  • Send to a friend  • Save in My Folder  • Save to citation manager  • Permissions  Citing Articles  • Citing articles on ISI (10)  • Contact me when this article is cited  Related Content  • Similar articles in JAMA  Topic Collections  • Oncology  • Drug Therapy, Other  • Alert me on articles by topic

Tracy Hampton, PhD

JAMA. 2004;292:419-422.

	Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

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 . . . [Full Text of this Article]