1. BRAF and RAS Mutations in Sporadic and Secondary Pyogenic Granuloma
Leopold Groesser, Eva Peterhof, Matthias Evert, Michael Landthaler, Mark Berneburg, Christian Hafner 
Journal of Investigative Dermatology 
Volume 136, Issue 2, Pages (February 2016)
DOI: /JID
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2. Figure 1
Clinical, histologic, and genetic analyses of PG (a and b) and nodular hypertrophies (c and d) in PWSs. (a) PG of subject 3 (Table 1) presenting as red polypoid tumor with a subtle collarette on a preexisting PWS. (b) Histologically, the PG shows compact vascular proliferation of solid, largely collapsed vascular structures. The BRAF c.1799T>A mutation is present in the PG, whereas the underlying PWS showed a wild-type sequence at codon 600 of BRAF. The PG and PWS both carry the GNAQ c.548G>A mutation. (c) Multiple papular lesions have developed on a PWS. (d) Histologically, the nodular lesion is composed of thin-walled vascular channels with varying lumina. The node is positive for the somatic GNAQ c.548G>A mutation but shows a wild-type sequence at codon 600 of BRAF. Peaks indicate the DNA antisense strand of the GNAQ gene and the DNA sense strand of the BRAF gene. Scale bar = 2 mm.
Journal of Investigative Dermatology  , DOI: ( /JID )
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3. Figure 2
Histology and corresponding RAS SNaPshot multiplex assay chromatograms of sporadic PG (a) and sporadic CA (b). (a) PG of subject 23 (Table 2) presenting as a dome-shaped lesion with a well-developed lobular architecture. The lesional tissue shows a KRAS c.37G>C mutation, whereas the adjacent epidermis revealed a wild-type sequence at codon 13 of KRAS. (b) CA of subject 18 (Table 3) presents as a dome-shaped lesion with insinuated lobules and thin-walled dilated vascular channels. Genetic analysis revealed a somatic HRAS c.182A>G mutation in the dermal vascular proliferation. Insets show a higher magnification of the respective lesions. Peaks indicate the DNA antisense strand of the respective genes. Scale bar = 2 mm.
Journal of Investigative Dermatology  , DOI: ( /JID )
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4. Figure 3
Immunohistochemical analysis of BRAF p.(Val600Glu) expression and localization in secondary and sporadic PGs. (a) Representative BRAF p.(Val600Glu) staining of a PG (subject 3 in Table 1) arisen on a PWS. Endothelial cells could clearly be identified as carriers of the BRAF p.(Val600Glu) mutation. (b) BRAF p.(Val600Glu) expression in endothelial cells of a sporadic PG (subject 17 in Table 2). (c) Representative negative (left) and positive (right) control staining of a PG with BRAF wild-type sequence and a melanoma with a BRAF p.(Val600Glu) mutation. Scale bar = 100 μm.
Journal of Investigative Dermatology  , DOI: ( /JID )
Copyright © 2015 The Authors Terms and Conditions