Russian Journal of Skin and Venereal DiseasesRussian Journal of Skin and Venereal Diseases1560-95882412-9097Eco-Vector3716710.18821/1560-9588-2016-19-5-283-286Research ArticleExpression of protein p27 in various forms of seborrheic keratosisAleksandrovaAlexandra K.Department of Pathological Anatomy; MD, PhDveter278@rambler.ruSukolinG. I-SmolynnikovaV. ADepartment of Pathological Anatomy-I.M. Sechenov First Moscow State Medical UniversityPolyclinic №1 of the Office of the President of the Russian Federation1510201619528328621072020Copyright © 2016, Eco-Vector2016The significant role in the pathogenesis of seborrheic keratosis (SK) plays the violation of the cell cycle regulation. According to the research unit the cell proliferation in acanthotic and irritated histological types of SK is regulated by p27 (Kip1), cyclin-dependent kinase inhibitor. Considering the variety of histological types of SK, definition of p27 expression will reveal the characteristic features of the cell cycle disorders and proliferation for each type of tumor. Material and Methods. Of the 102 tumors from patients with SK, according to the results of histological examination, were selected 10 specimens of each histological types of SK: acanthotic, hyperkeratotic, adenoid, irritated, and clonal. We assessed all specimens for p27 (Kip1) expression using immunohistochemistry (monoclonal antibody p27 at a dilution of 1:20 (Novocastra Laboratories Ltd.). Three skin biopsy samples of healthy individuals were included. Results. Severe diffuse nuclear expression of p27 was present in all cases of adenoid, irritated, and 4 cases of clonal histological types of SK. In other tumor types positive reaction with monoclonal antibody to p27 was reduced as compared with healthy skin were recorded single positively stained nuclei of basal cells. Conclusions. Thus, we have found a violation of p27 protein expression in all types of seborrheic keratosis as with the excess (adenoid, irritated, clonal SK type) and in p27 protein deficiency (acanthotic, hyperkeratotic) normal course of cell cycle phases is broken. This leads to the disappearance of control over the cell proliferative activity and apoptosis, facilitating a slow, uncontrolled growth of SK cells.seborrheic keratosisp27cell cycleсеборейный кератозэкспрессия белка р27клеточный цикл[Wolff К., Goldsmith L., Katz S.I., Gilchrest B.A., Paller A.S., Leffell D.J., eds. Fitzpatrick s Dermatology in General Medicine, 7th ed. New York: McGraw-Hill Medical; 2008. vol. 1: 635-6.][Kwon O.S., Hwang E.J., Bae J.H., Park H.E., Lee J.C., Youn J.I., Chung J.H. Seborrheic keratosis in the Korean males: causative role of sunlight. Photodermatol. Photoimmunol. Photomed. 2003; 19(2): 73-80.][Elder D., Elenitsas R., Johnson B., Murphy G.F., Xu X., eds. Lever’s histopathology of the skin. 10th ed. Philadelphia: Lippincott-Raven; 2008: 795-8.][Kim H.S., Park E.J., Kwon I.H., Kim K.H., Kim K.J. Clinical and histopathologic study of benign lichenoid keratosis on the face. Am. J. Dermatopathol. 2013; 35(7): 738-41.][Mohamed M., Amri M., Njim L., Jribi M., Zakhama A., Zili J. Pigmented keratosis on the face. Ann. Dermatol. Venereol. 2013; 140(5): 390-2.][Hafner C., van Oers J.M., Hartmann A., Landthaler M., Stoehr R., Blaszyk H., et al. High frequency of FGFR3 mutations in adenoid seborrheic keratoses. J. Invest. Dermatol. 2006; 126(11): 2404-7.][Bruecks A.K., Kalia S., Trotter M.J. Overexpression of p27 KIP1 in seborrheic keratosis. J. Cutan. Med. Surg. 2007; 11(5): 174-8.][Ruas M., Gregory .F, Jones R., Poolman R., Starborg M., Rowe J., et al. CDK4 and CDK6 delay senescence by kinase-dependent and p16INK4a-independent mechanisms. Mol. Cell Biol. 2007; 27(12): 4273-82.][Seargent J.M., Loadman P.M., Martin S.W., Naylor B., Bibby M.C., Gill J.H. Expression of matrix metalloproteinase-10 in human bladder transitional cell carcinoma. Urology. 2005; 65(4): 815-20.][Morgan D. Cell Cycle: Principals of Control. London: New Science Press Ltd.; 2007: 145-6.][Mitrea D.M., Yoon M.K., Ou L., Kriwacki R.W. Disorder-function relationships for the cell cycle regulatory proteins p21 and p27. Biol. Chem. 2012; 393(4): 259-74.][Pellegata N.S., Quintanilla-Martinez L., Siggelkow H., Samson E., Bink K., Hofler H., et al. Germ-line mutations in p27 Kip1 cause a multiple endocrine neoplasia syndrome in rats and humans. Proc. Natl. Acad. Sci. U.S.A. 2006; 103(42): 15558-63.]