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Abstract
Clinical inhibition of the epidermal growth factor receptor (EGFR) results in stereotypic papulopustular eruptions, bacterial superinfection of the skin with Staphylococcus aureus (S. aureus) and diarrhea. These stigmatizing side effects severely deteriorate patients’ wellbeing and therapy adherence. Hence, the identification and characterization of EGFR dependent anti-microbial defense mechanisms is of utter importance to improve our capability to treat those adverse barrier effects to increase patients’ quality of life and enhance EGFR targeted cancer therapy efficacy.
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