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Mutational Analysis of BRAF Inhibitor–Associated Squamoproliferative Lesions  Britt Clynick, Tania Tabone, Kathryn Fuller, Wendy Erber, Katie Meehan, Michael.

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Presentation on theme: "Mutational Analysis of BRAF Inhibitor–Associated Squamoproliferative Lesions  Britt Clynick, Tania Tabone, Kathryn Fuller, Wendy Erber, Katie Meehan, Michael."— Presentation transcript:

1 Mutational Analysis of BRAF Inhibitor–Associated Squamoproliferative Lesions 
Britt Clynick, Tania Tabone, Kathryn Fuller, Wendy Erber, Katie Meehan, Michael Millward, Benjamin A. Wood, Nathan T. Harvey  The Journal of Molecular Diagnostics  Volume 17, Issue 6, Pages (November 2015) DOI: /j.jmoldx Copyright © 2015 American Society for Investigative Pathology and the Association for Molecular Pathology Terms and Conditions

2 Figure 1 Graphical representation of the number of lesions containing mutations for each of the genes for which at least one mutation was identified. A: All lesions. B: BRAF inhibitor (BRAFi)–associated lesions. BAVK, BRAF inhibitor–associated verrucous keratosis; KA, keratoacanthoma; SCC, squamous cell carcinoma. The Journal of Molecular Diagnostics  , DOI: ( /j.jmoldx ) Copyright © 2015 American Society for Investigative Pathology and the Association for Molecular Pathology Terms and Conditions

3 Figure 2 Representative examples of both the hematoxylin and eosin (H&E) appearances and immunohistochemical (IHC) staining for the phosphorylated form of extracellular signal–related kinase (pERK) in a BRAF inhibitor–associated verrucous keratosis (A and B, respectively), a keratoacanthoma (C and D, respectively), and a squamous cell carcinoma (E and F, respectively). All three lesions originated from patients undergoing treatment with a BRAF inhibitor. A, C, and E: H&E staining. B, D, and F: IHC staining for pERK. The Journal of Molecular Diagnostics  , DOI: ( /j.jmoldx ) Copyright © 2015 American Society for Investigative Pathology and the Association for Molecular Pathology Terms and Conditions

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