Open Access

SRC in human carcinogenesis

Salvatore V. Russello1,Scott K. Shore1,*
Fels Institute for Cancer Research & Department of Biochemistry, Temple University School of Medicine, 3307 N. Broad Street, Philadelphia PA 19140, USA
DOI: 10.2741/1138 Volume 8 Issue 6, pp.1068-1073
Published: 01 September 2003
(This article belongs to the Special Issue Tyrosine protein phosphorylation in cell signaling)
*Corresponding Author(s):  
Scott K. Shore

The signaling machinery in cells is a complex, multi-factorial network of cross-talking proteins that enables dynamic communication between upstream causal factors and downstream effectors. Non-receptor tyrosine kinases, including Src, are the intermediates of information transfer, controlling pathways as diverse as cell growth, migration, death, and genome maintenance. When expressed as viral genes these proteins are potent carcinogens, yet analogous genetic alterations are rarely observed in human tumors. In seeking to characterize the role of the non-receptor tyrosine kinase Src in neoplasia, arguments can be made that the consequences of mutation, or perturbations in the activity or expression of this protein is a determinative factor in clinical prognosis and pathogenicity. In a variety of tumor types including those derived from the colon and breast, the Src non-receptor tyrosine kinase is either overexpressed or constitutively active in a large percentage of the tumors. Increased expression or activity of Src correlates with the stage and metastatic potential of some neoplasia.

Key words

Non-Receptor Tyrosine Kinase, Receptor Tyrosine Kinase, Phosphorylation, Colon Cancer, Breast Cancer, Review

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Salvatore V. Russello, Scott K. Shore. SRC in human carcinogenesis. Frontiers in Bioscience-Landmark. 2003. 8(6); 1068-1073.