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Dermatologic toxicities to targeted cancer therapy: shared clinical and histologic adverse skin reactions
Author(s) -
Curry Jonathan L.,
TorresCabala Carlos A.,
Kim Kevin B.,
Tetzlaff Michael T.,
Duvic Madeleine,
Tsai Kenneth Y.,
Hong David S.,
Prieto Victor G.
Publication year - 2014
Publication title -
international journal of dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.677
H-Index - 93
eISSN - 1365-4632
pISSN - 0011-9059
DOI - 10.1111/ijd.12205
Subject(s) - medicine , cetuximab , actinic keratosis , skin cancer , targeted therapy , cancer , keratoacanthoma , vemurafenib , dermatology , sorafenib , egfr inhibitors , psoriasis , mek inhibitor , erlotinib , gefitinib , trametinib , cancer research , tyrosine kinase inhibitor , epidermal growth factor receptor , pathology , mapk/erk pathway , kinase , colorectal cancer , basal cell , metastatic melanoma , hepatocellular carcinoma , biology , microbiology and biotechnology
Background Dermatologic toxicities ( DT ) to targeted cancer therapy may present as inflammatory dermatoses, keratoses, and as benign and malignant squamous proliferations. Methods Published reports of DT with cancer therapy with epidermal growth factor receptor ( EGFR ), tyrosine kinase ( TK ), MEK , PI 3K, AKT , and BRAF inhibitors were reviewed. Results DT associated with targeted cancer therapy demonstrated similar reactions and may be grouped as (i) DT as cutaneous inflammation, and (ii) DT as cutaneous epithelial proliferation. EGFR inhibitor, cetuximab, and MEK inhibitors, selumetinib and trametinib, demonstrated papulopustular rash with a suppurative folliculitis in 83%, 93%, and 80% of the patients on therapy, respectively. Common DT with EGFR inhibitors erlotinib and tyrosine kinase inhibitor sorafenib were hand–foot skin reactions in 30–60% of patients on therapy. PI 3K inhibitor BKM ‐120 and AKT inhibitor MK 2206 produced maculopapular eruptions seen as dermal hypersensitivity reaction on the skin biopsy. RAF inhibitors vemurafenib and sorafenib were associated with a variety of cutaneous epithelial proliferations (keratosis pilaris, seborrheic keratosis, verruca vulgaris, actinic keratosis, keratoacanthoma, and squamous cell carcinoma. Conclusion Various anticancer agents may target similar cellular compounds and/or cell signaling pathways thus share similar clinical and histologic features of DT . The knowledge of the overlap of DT with different types of targeted cancer therapy will assist in evaluation of cutaneous reactions.