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Sci. STKE, 22 May 2007
Vol. 2007, Issue 387, p. tw180
[DOI: 10.1126/stke.3872007tw180]

EDITORS' CHOICE

Medicine Smart Drugs, Smarter Tumors

Paula A. Kiberstis

Science, AAAS, Washington, DC 20005, USA

A promising class of "smart" cancer drugs work by inhibiting specific tyrosine kinases linked to uncontrolled growth. Gefitinib and erlotinib, drugs that target the kinase activity of the epidermal growth factor receptor (EGFR), can be very effective when initially administered to lung cancer patients whose tumors contain activating mutations in the EGFR gene. Almost inevitably, however, these tumors develop resistance to the drugs and begin to regrow. Engelman et al. find that drug resistance in a subset of these tumors is caused by amplification of the MET oncogene, an event that in turn activates, via a different route, the same cellular signaling pathway originally activated by the mutant EGFR.

J. A. Engelman, K. Zajnullahu, T. Mitsudomi, Y. Song, C. Hyland, J. O. Park, N. Lindeman, C.-M. Gale, X. Zhao, J. Christensen, T. Kosaka, A. J. Holmes, A. M. Rogers, F. Cappuzzo, T. Mok, C. Lee, B. E. Johnson, L. C. Cantley, P. A. Jänne, MET Amplification leads to gefitinib resistance in lung cancer by activating ERBB3 signaling. Science 316, 1039-1043 (2007). [Abstract] [Full Text]

Citation: P. A. Kiberstis, Smart Drugs, Smarter Tumors. Sci. STKE 2007, tw180 (2007).

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Science Signaling. ISSN 1937-9145 (pre-2008: Science's STKE. ISSN 1525-8882)