The role of polymorphism of the epidermal growth factor gene in the formation of severe manifestations of skin toxicity caused by the use of EGFR inhibitors

Abstract

Epidermal growth factor receptor (EGFR) inhibitors are widely used to treat various types of cancer, such as non-small cell lung cancer, head and neck cancer, breast cancer, pancreatic cancer, colorectal cancer. During treatment, class-mediated effects such as skin toxicity, interstitial lung disease, hepatotoxicity, ocular toxicity, hypomagnesemia, stomatitis, and diarrhea may occur. The role of epidermal growth factor and its receptors in the vital activity of keratinocytes is key. Dermatological undesirable effects occur in 60–90% of patients, and often persist throughout the entire period of EGFR inhibitor therapy.
 Currently, studies of biomarkers predicting the severity of skin complications of EGFR inhibitor therapy are extremely limited. Thus, it is relevant to study genetic markers reliably associated with the development of severe skin toxicity against the background of EGFR inhibitor therapy, because the EGFR signaling pathway is important for maintaining normal physiological function of the skin. The development of severe skin reactions leads to a reduction in the dose or discontinuation of EGFR inhibitors in the treatment of cancer. Recently, progress has been made in studies of the cutaneous toxicity of EGFR inhibitors.
 Here we briefly describe the mechanism of skin toxicity caused by EGFR inhibitors, current data on the relationship of gene polymorphism and severity of manifestations of undesirable dermatological phenomena.