Grb7-based molecular therapeutics in cancer.
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.
Department of Surgery and the Vermont Cancer Center, University of Vermont School of Medicine, Given Medical Building, Burlington, VT 05405, USA. Stephanie.Pero@uvm.edu
Stephanie C
SC
Pero
Roger J
RJ
Daly
David N
DN
Krag
D016503:Drug Delivery Systems; D051382:GRB7 Adaptor Protein / Q000037:antagonists & inhibitors / Q000737:chemistry / Q000235:genetics / Q000502:physiology*; D015972:Gene Expression Regulation, Neoplastic; D006801:Humans; D009369:Neoplasms / Q000188:drug therapy* / Q000209:etiology; D018909:src Homology Domains
D051382:GRB7 Adaptor Protein