Numerous studies have demonstrated that tyrosine kinases, which phosphorylate tyrosine residues in protein that could be associated with either transmembrane receptor-linked proteins or non-receptor cytoplasmic proteins, play critical roles in the development and progression of many epithelial malignancies, including colorectal cancer.^6–10 There is an increasing body of evidence to support the concept that the malignant behaviour of some tumours is sustained by deregulated activation of certain growth factor receptors. Such deregulation could be structural alterations of the receptor itself,^11,12 the establishment of an autocrine loop, whereby the cells produce growth factors that stimulate their own growth,^13–15 or the loss of suppressor of growth factor receptor function. The receptors with intrinsic tyrosine kinases are activated following binding of their growth factors. One of the best studied receptor signalling systems from this family is that controlled by the epidermal growth factor receptor (EGFR) and its family members, whose expression and enzyme activity have been linked to a number of malignancies, including cancers of the colon and breast.^16–19 In addition, a growing number of studies have implicated the insulin-like growth factor (IGF)/IGF-receptor-1 (IGF-1R) and vascular endothelial growth factor (VEGF)/VEGF-receptor (VEGFR) systems, as well as c-Src, a nonreceptor tyrosine kinase, in the development and progression of colorectal cancer.^20–25 Recent studies also suggest platelet-derived growth factor receptor (PDGFR), which possesses tyrosine kinase activity, to be involved in the progression of colorectal cancer.²⁶ As it is beyond the scope of this article to describe the role of all growth factor receptors and non-receptor tyrosine kinases in colorectal cancer, the focus will be on EGFR (and its familymembers) and c-Src.

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