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Grb7-based molecular therapeutics in cancer

Published online by Cambridge University Press:  13 February 2004

Stephanie C. Pero ,
Roger J. Daly  and
David N. Krag
Stephanie C. Pero
Affiliation:
Department of Surgery and the Vermont Cancer Center, University of Vermont School of Medicine, Given Medical Building, Burlington, VT 05405, USA.
Roger J. Daly
Affiliation:
Cancer Research Program, Garvan Institute of Medical Research, St Vincent's Hospital, Sydney, New South Wales, 2010, Australia.
David N. Krag
Affiliation:
Department of Surgery and the Vermont Cancer Center, University of Vermont School of Medicine, Given Medical Building, Burlington, VT 05405, USA.
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Abstract

Traditional anti-cancer drugs preferentially kill rapidly growing tumour cells rather than normal cells. However, most of these drugs have no preferential selection towards cancer cells and are taken up by the whole body, resulting in significant adverse side effects. Therapeutic molecules that could specifically inhibit undesirable phenotypes are an attractive way of eliminating cancer cells. There is a widespread effort to develop inhibitors against signal transduction molecules that play a key role in the proliferative, migratory and invasive properties of a cancer cell. Grb7 is an adaptor-type signalling protein that is recruited via its Src-homology 2 (SH2) domain to a variety of tyrosine kinases. Grb7 is overexpressed in breast, oesophageal and gastric cancers, and may contribute to the invasive potential of cancer cells. Molecular interactions involving Grb7 therefore provide attractive targets for therapeutic intervention.

Keywords

Grb7SH2 domainErbB2targeted therapeuticssignal transduction inhibitorpeptidecancerreceptor tyrosine kinase
Type
Review Article
Information
Expert Reviews in Molecular Medicine , Volume 5 , Issue 14 , 10 May 2003 , pp. 1 - 11
Copyright
© Cambridge University Press 2003

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