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Better understanding of the mechanisms underlying cancer development has lead to the development of new anti-cancer drugs aimed at specific molecular targets. Because cancer is a heterogeneous disease, however, many of these new drugs work only in a subset of patients. They are also expensive, and they can have serious side effects. Scientists are therefore trying to find ways to predict who will benefit from a particular drug, so that they can better weigh the risks and benefits for an individual patient. In an article in the current issue of the international open-access medical journal PLoS Medicine, William Pao, Harold Varmus, and colleagues from Memorial Sloan Kettering Cancer Center in New York report results that might lead to more "targeted therapy" for lung cancer patients.
The researchers had previously shown that the epidermal growth factor (EGF) receptor, a tyrosine kinase, is often mutated in non-small-cell lung cancers, and that tumors that harbor such mutations are sensitive to two drugs called gefitinib and erlotinib. In the new study, they focused on a signaling protein called KRAS. The KRAS gene is also often mutated in lung cancers, but very few cancers have mutations in both the EGF receptor and the KRAS gene. The researchers found that those patients whose tumors had KRAS mutations had not shown an anti-tumor response when they were treated with either erlotinib or gefitinib.
These findings need to be validated by additional studies. If they are confirmed, it means that doctors should analyze tumors for mutations in the EGF receptor and KRAS before they decide whom to treat with erlotinib or gefitinib.
Citation: Pao W, Wang T, Riely G, Miller V, Pan Q, et al. (2005) KRAS mutations and primary resistance of lung adenocarcinomas to gefitinib or erlotinib. PLoS Med 2 (1): e17.
CONTACT:
William Pao
MSKCC
Medicine/Cancer Biology & Genetics
Varmus Lab - Box 62
1275 York Avenue
New York, NY USA 10021
1-212-639-6193
1-212-717-3125 (fax)
paow@mskcc.org
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