BRAF Expression in Keratoacanthoma
Abstract
Objective: Mutations in genes encoding proteins along the RAS-RAF-MEK-ERK pathway have been detected in a variety of tumor entities, including malignant melanoma, thyroid, colon, over carcinomas and some sarcomas. The increased activity of BRAF V600E leads to downward signalization activation via mitogen-activated protein kinase (MAPK), which plays an important role as cell growth, differentiation and survival regulator. Latest data show BRAF undergoes mutation in nearly 7% of cancers and this situation makes BRAF another important oncogene in this pathway. We aimed to evaluate the relationship between keratacanthoma and BRAF expression.
Methods: 28 cases of keratocanthomas were included in this study. Sections were taken from the selected blocks with a thickness of 3 microns with poly-lysine coating. BRAF antibody was applied to the tissues. The obtained preparations were evaluated by light microscopy. It was rated according to the degree of staining in epidermis.
Results: Areas showing cytoplasmic staining with BRAF were evaluated in sections. It was observed that there was no staining in the keratocanthomas, and staining in sebaceous glands and sweat glands in peripheral basal cells. It was also noted that the sweat glands had more stain than the sebaceous glands. The cases included 18 males and 10 females with ages varying from 33 to 85 years. The duration of the lesions was between one month and one year. Lesion dimensions varied from 5 to 70 mm, with mean size of 21 mm. There were 14 cases (50%) with head and neck localization, and 14 cases (50%) with localization other than the head and neck.
Conclusion: As a result, it has been concluded that BRAF mutation may not be involved in keratoacanthoma.
Keywords
References
- Abildgaard C, Guldberg P. Molecular drivers of cellular metabolic reprogramming in melanoma. Trends Mol Med 2015;21:164-71.
- Adackapara CA, Sholl LM, Barletta JA, Hornick JL Immunohistochemistry using the BRAF V600E mutation-specific monoclonal antibody VE1 is not a useful surrogate for genotyping in colorectal adenocarcinoma. Histopathology. 2013 Aug;63(2):187-93.
- Aksoy B, Aksoy HM, Akın O. Keratoacanthoma in an acrochordon. Turkderm-Turk Arch Dermatol Venereolgy 2017;51:24-5.
- Alloo A, Garibyan L, LeBoeuf N, Lin G, Werchniak A, Hodi FS Jr, et al. Photodynamic therapy for multiple eruptive keratoacanthomas associated with vemurafenib treatment for metastatic melanoma. Arch Dermatol.2012 Mar;148(3):363-6.
- Anforth R, Tembe V, Blumetti T, Fernandez-Peñas P. Mutational analysis of cutaneous squamous cell carcinomas and verrucal keratosis in patients taking BRAF inhibitors. Pigment Cell Melanoma Res. 2012;25(5):569-72.
- Arnault JP, Mateus C, Escudier B, Tomasic G, Wechsler J, Hollville E, et al. Skin tumors induced by sorafenib; paradoxic RAS-RAF pathway activation and oncogenic mutations of HRAS, TP53, and TGFBR1. Clin Cancer Res. 2012 Jan 1;18(1):263-72.
- Bell D, Aung P, Prieto VG, Ivan D. Next-Generation Sequencing Reveals Rare Genomic Alterations in Aggressive Digital Papillary Adenocarcinoma. Annals of Diagnostic Pathology. 2015; 19(6): 381–384.
- Chauhan A, Chaudhary S, Agnihotri PG, Aadithya B. A solitary crateriform ulcer of the lower lip: a case report with review of literature. Indian J Dermatol. 2011; 56: 435–438.
- Clausen OP, Aass HC, Beigi M, Purdie KJ, Proby CM, Brown VL, et al. Are keratoacanthomas variants of squamous cell carcinomas? A comparison of chromosomal aberrations by comparative genomic hybridization. J Invest Dermatol. 2006; 126: 2308–2315.
- Clynick B, Tabone T, Fuller K, Erber W, Meehan K, Millward M, et al. Mutational Analysis of BRAF Inhibitor-Associated Squamoproliferative Lesions.J Mol Diagn. 2015 Nov;17(6):644-51.