Skin toxicity caused by EGFR antagonists-an autoinflammatory condition triggered by deregulated IL-1 signaling?
Acneiform skin eruptions associated with sterile inflammation frequently accompany pharmacological inhibition of signaling through the epidermal growth factor receptor (EGFR) in cancer patients. Here we discuss possible pathogenic mechanisms for this phenomenon linked to control of inflammatory mediators by EGFR blockade in keratinocytes of the outer root sheath of the hair follicle. This discussion is focused on the putative role of EGFR activation in restraining interleukin (IL)-1-dependent inflammatory networks at the hair follicle.
Rodeck
Ulrich
U
Department of Dermatology, Cutaneous Biology and Kimmel Cancer Center, Thomas Jefferson University, Philadelphia, Pennsylvania, USA. ulrich.rodeck@mail.tju.edu
D000970:Antineoplastic Agents / Q000009:adverse effects; D003875:Drug Eruptions / Q000209:etiology* / Q000503:physiopathology; D066246:ErbB Receptors / Q000037:antagonists & inhibitors*; D018859:Hair Follicle / Q000187:drug effects / Q000503:physiopathology; D006801:Humans; D018836:Inflammation Mediators / Q000502:physiology; D007375:Interleukin-1 / Q000502:physiology*; D015603:Keratinocytes / Q000187:drug effects / Q000502:physiology; D009369:Neoplasms / Q000188:drug therapy; D015398:Signal Transduction / Q000187:drug effects
D000970:Antineoplastic Agents; D018836:Inflammation Mediators; D007375:Interleukin-1; C512478:EGFR protein, human; D066246:ErbB Receptors