Rash and skin toxicity (acneiform rash, paronychia)
Skin reactions from cancer drugs, ranging from the acne-like rash that nearly everyone on an EGFR inhibitor gets (a sign the drug is working) to painful nail-fold infections, itching, and rare severe blistering reactions.
EGFR inhibitors (cetuximab, panitumumab, osimertinib, amivantamab) cause acneiform rash, paronychia and dry skin in most patients through on-target blockade in skin, managed with prophylactic doxycycline, topical steroids and moisturisers; the rash correlates with response. MEK and BRAF inhibitors, ADCs (enfortumab vedotin can cause severe, occasionally fatal skin reactions), immunotherapy (maculopapular rash, pruritus, vitiligo in melanoma, which predicts response), and chemotherapy (hand-foot syndrome, hyperpigmentation) all have characteristic patterns. Severe cutaneous adverse reactions (Stevens-Johnson syndrome, toxic epidermal necrolysis) are rare but require permanent discontinuation. Skin toxicity is a leading cause of dose reduction and of visible distress for patients.
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- InstitutionVanderbilt-Ingram Cancer Center
- TermOn-target resistance mutations (gatekeeper, solvent-front, compound)