Note to users. If you're seeing this message, it means that your browser cannot find this page's style/presentation instructions -- or possibly that you are using a browser that does not support current Web standards. Find out more about why this message is appearing, and what you can do to make your experience of our site the best it can be.


Sci. STKE, 4 February 2003
Vol. 2003, Issue 168, p. tw55
[DOI: 10.1126/stke.2003.168.tw55]

EDITORS' CHOICE

Cancer Biology Two Means to a Bad End

Gastrointestinal stromal tumors (GISTs) have recently attracted much attention because they are exceptionally sensitive to the new cancer drug Gleevec, which inhibits the oncogenic KIT receptor tyrosine kinase that is aberrantly expressed in many of these tumors. Heinrich et al. have now examined GISTs with normal KIT function and find that these tumors harbor activating mutations in a gene that encodes a related tyrosine kinase, platelet-derived growth factor receptor-A (PDGFRA). Tumors with mutations in KIT or PDGFRA have similar cytogenetic profiles and display activation of the same downstream signaling pathways. These results reinforce the notion that mutations in distinct genes can activate common cellular pathways that drive cancer development.

M. C. Heinrich, C. L. Corless, A. Duensing, L. McGreevey, C.-J. Chen, N. Joseph, S. Singer, D. J. Griffith, A. Haley, A. Town, G. D. Demetri, C. D. M. Fletcher, J. A. Fletcher, PDGFRA activating mutations in gastrointestinal stromal tumors. Science 299, 708-710 (2003). [Abstract] [Full Text]

Citation: Two Means to a Bad End. Sci. STKE 2003, tw55 (2003).



To Advertise     Find Products


Science Signaling. ISSN 1937-9145 (online), 1945-0877 (print). Pre-2008: Science's STKE. ISSN 1525-8882