Keratoacanthoma Shares Driver Mutations with Cutaneous Squamous Cell Carcinoma  Young H. Lim, Jonathan M. Fisher, Marcus W. Bosenberg, Keith A. Choate, Christine J. Ko  Journal of Investigative Dermatology  Volume 136, Issue 8, Pages 1737-1741 (August 2016) DOI: 10.1016/j.jid.2016.04.002 Copyright © 2016 The Authors Terms and Conditions

Figure 1 Clinical and histologic features of KA and driver mutation profiles. Clinical presentation and histopathology (original magnification ×4) of (a, b) KA100, (c, d) KA101, (e, f) KA102, (g, h) KA103, (i, j) KA104, and (k, l) KA105. All lesions are crateriform with a pink, stretched border and central keratin. The partial biopsy samples show epithelium of varying thickness and atypia bordering central keratin. The greatest atypia is present in KA104 (j). (m) Mutations in known driver genes of cutaneous squamous cell carcinoma were found in all growing KAs (samples in red) and 50% of vemurafenib-induced squamous lesions but were absent in regressing lesions (samples in green). Paired lesions at different stages of KA (asterisks) showed loss of driver mutation during regression. Keratinocytic regions were targeted for sampling tissue for DNA to avoid significant admixture with inflammatory infiltrates (plus signs). Scale bars = 50 μm. KA, keratoacanthoma; VSL, vemurafenib-induced squamoproliferative lesion. Journal of Investigative Dermatology 2016 136, 1737-1741DOI: (10.1016/j.jid.2016.04.002) Copyright © 2016 The Authors Terms and Conditions