Epidermal growth factor receptor (EGFR) is a member of the HER family of tyrosine kinase cell-surface receptors that are dysregulated in many types of tumor; its expression has been associated with a poor prognosis in colon cancer.1 There are at least two opportunities to interfere with EGFR signaling that are being exploited clinically.2 In one approach, the extracellular receptor domain is bound by antibodies, such as cetuximab, that block ligand-mediated dimerization and subsequent activation of the receptor. In the second, the tyrosine kinase domain is bound by drugs that inhibit phosphorylation, such as gefitinib and erlotinib.Irinotecan is a topoisomerase . . .
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Erlichman et al. (2004) studied this question.
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