Ann Dermatol.  2017 Jun;29(3):373-376. 10.5021/ad.2017.29.3.373.

p16(INK4a) Expression in Porokeratosis

Affiliations
  • 1Department of Dermatology, Kyushu University, Fukuoka, Japan. furue@dermatol.med.kyushu-u.ac.jp
  • 2Division of Skin Surface Sensing, Department of Dermatology, Kyushu University, Fukuoka, Japan.
  • 3Research and Clinical Center for Yusho and Dioxin, Kyushu University, Fukuoka, Japan.

Abstract

No abstract available.


MeSH Terms

Cyclin-Dependent Kinase Inhibitor p16*
Porokeratosis*
Cyclin-Dependent Kinase Inhibitor p16

Figure

  • Fig. 1 Immunohistological expression of p16INK4a in disseminated superficial porokeratosis. (A) p16INK4a expression is present in the periphery (dotted rectangle) and the center of the lesion. The perilesional normal epidermis lacks positive signals. (B) Cornoid lamella is negatively stained with p16INK4a. Some keratinocytes beneath the cornoid lamella are positive for p16INK4a (arrows). (C) p16INK4a-immunopositive keratinocytes are detected in the central area of the lesion. (D) Cornoid lamella is negatively stained with p16INK4a. Some keratinocytes beneath the cornoid lamella are positive for p16INK4a (arrows). M: melanin granules. Bar: 100 µm.

  • Fig. 2 Immunohistological expression of p16INK4a in porokeratosis of Mibelli. (A) p16INK4a expression is present in the periphery (dotted rectangle) and the center of the lesion. The perilesional normal epidermis is completely negative for p16INK4a. (B) Cornoid lamella is negatively stained with p16INK4a. Some keratinocytes beneath the cornoid lamella are positive for p16INK4a (arrows). Vacuolated keratinocytes (asterisks) are also positively stained. (C) p16INK4a-immunopositive keratinocytes are detected in the central area of the lesion. M: melanin granules. Bar: 100 µm.


Reference

1. Sertznig P, von Felbert V, Megahed M. Porokeratosis: present concepts. J Eur Acad Dermatol Venereol. 2012; 26:404–412.
Article
2. Sharpless NE, Sherr CJ. Forging a signature of in vivo senescence. Nat Rev Cancer. 2015; 15:397–408.
Article
3. Mowla SN, Lam EW, Jat PS. Cellular senescence and aging: the role of B-MYB. Aging Cell. 2014; 13:773–779.
Article
4. Scola N, Skrygan M, Wieland U, Kreuter A, Gambichler T. Altered gene expression in squamous cell carcinoma arising from congenital unilateral linear porokeratosis. Clin Exp Dermatol. 2012; 37:781–785.
Article
5. Tsujita J, Kaku Y, Ichiki T, Eto A, Maemura H, Otsuka A, et al. Immunohistological expression of p16INK4a is commonly present both in benign and malignant sweat gland neoplasias. Fukuoka Igaku Zasshi. 2015; 106:323–329.
6. Arranz-Salas I, Sanz-Trelles A, Ojeda DB. p53 alterations in porokeratosis. J Cutan Pathol. 2003; 30:455–458.
Article
7. Park HR, Min SK, Cho HD, Kim KH, Shin HS, Park YE. Expression profiles of p63, p53, survivin, and hTERT in skin tumors. J Cutan Pathol. 2004; 31:544–549.
Article
8. Cheng AS, Karnezis AN, Jordan S, Singh N, McAlpine JN, Gilks CB. p16 immunostaining allows for accurate subclassification of vulvar squamous cell carcinoma into HPV-associated and HPV-independent cases. Int J Gynecol Pathol. 2016; 35:385–393.
Article
9. Tschandl P, Berghoff AS, Preusser M, Pammer J, Pehamberger H, Kittler H. Impact of oncogenic BRAF mutations and p16 expression on the growth rate of early melanomas and nevi in vivo. Br J Dermatol. 2016; 174:364–370.
Article
10. Zhang C, Toulev A, Kamarashev J, Qin JZ, Dummer R, Döbbeling U. Consequences of p16 tumor suppressor gene inactivation in mycosis fungoides and Sézary syndrome and role of the bmi-1 and ras oncogenes in disease progression. Hum Pathol. 2007; 38:995–1002.
Article
Full Text Links
  • AD
Actions
Cited
CITED
export Copy
Close
Share
  • Twitter
  • Facebook
Similar articles
Copyright © 2024 by Korean Association of Medical Journal Editors. All rights reserved.     E-mail: koreamed@kamje.or.kr