Elucidation of mechanism of drug eruption due to epidermal growth factor receptor tyrosine kinase inhibitors

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Epidermal growth factor receptor tyrosine kinase(EGFR-TK) is a transducer of mitogenic signals, and is involved in the pathogenesis and progression of a number of cancers, including non-small cell lung cancer(NSCLC). Gefitinib is an EGFR-TK inhibitor that is clinically used to treat NSCLC ; however, this drug frequently causes adverse effects, including skin eruptions. The mechanism underlying these skin reactions is elusive, although it is assumed that they are caused by the inhibition of EGFR-TK signaling in epidermal and adnexal cells. In this study, we demonstrate that IL-1-mediated signaling is activated to induce the high expression of CCL2 and CCL5 via reduction of IL-1R2 in the skin lesions caused by gefitinib.