Recent developments related to the EGFR as a target for cancer chemotherapy.

Inhibition of the epidermal growth factor receptor as a target for cancer chemotherapy has proven to be an effective treatment in both preclinical and clinical settings. Recent work has indicated that the presence of somatic mutations in the tyrosine kinase domain of the epidermal growth factor receptor is a major determinant of the response to the tyrosine kinase inhibitors gefitinib and erlotinib. However, this is not the full story, and further work is needed to identify the factors underlying the response in those who do not carry mutations. Mechanisms of innate and acquired resistance to epidermal growth factor receptor inhibitors are also topics under investigation. Crosstalk between the epidermal growth factor receptor and other growth factor receptors involved in tumorigenesis has been implicated, along with downstream signalling molecules such as Ras, Braf and PTEN. A full understanding of these mechanistic aspects could lead to the identification of useful combinations of inhibitors of novel targets.