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Claudin and p53 expression in vulvar lichen sclerosus and squamous-cell carcinoma
  1. José Carlos Sadalla1,
  2. Sílvia Vanessa Lourenço2,
  3. Mirian Nacagami Sotto2,
  4. Edmund Chada Baracat1,
  5. Jesus Paula Carvalho1
  1. 1Department of Gynecology, Faculdade de Medicina, Universidade de São Paulo, São Paulo, Brazil
  2. 2Department of Dermatology, Faculdade de Medicina, Universidade de São Paulo, São Paulo, Brazil
  1. Correspondence to José Carlos Sadalla, Department of Gynecology, Instituto Central do Hospital das Clinicas da Faculdade de Medicina da Universidade de São Paulo, Av Dr Eneas de Carvalho Aguiar, 255. São Paulo, Brazil; jcsadalla{at}gmail.com

Abstract

Aims Vulvar squamous-cell carcinoma (SCC) is a rare gynaecological cancer. Vulvar SCC has been shown to develop from vulvar intraepithelial neoplasias, which are related to lichen sclerosus (LS). Most studies to date have compared vulvar SCC with LS only morphologically, but no detailed molecular analysis has been performed. The objective was to compare claudin and p53 expression in these diseases and determine if there was any association with expression and vulvar SCC progression.

Methods Immunohistochemical analysis was performed in order to determine expression of p53 and claudin 1, 2, 3, 4, 5, 7 and 11 in human vulvar tissue samples from LS, SCC and control patients.

Results Claudin 1, 2, 3, 4 and 5 were expressed comparably in the three groups. Claudin 7 and 11 expression was significantly decreased in LS and SCC samples compared with the control group. Expression of p53 was significantly increased in SCC and LS patient samples compared with the control group.

Conclusions Claudin 7 and 11 were not expressed in LS and SCC. However, there was no significant difference in expression of any of the claudins between the LS and SCC samples. Furthermore, p53 expression is the highest in SCC patients and lowest in the control group. However, expression of p53 did not vary between samples from isolated LS and LS associated SCC patients, suggesting that increased p53 expression is not the determining factor in the progression of LS lesions to SCC.

  • Vulvar neoplasms
  • vulvar lichen sclerosus
  • tight junctions
  • p53
  • immunohistochemistry
  • mutation
  • cell adhesion molecules
  • carcinoma
  • gynaecological pathology
  • tumour markers

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Footnotes

  • Competing interests None.

  • Ethics approval Ethics approval was provided by the Institutional Ethics Committee of Hospital das Clínicas da Universidade de São Paulo.

  • Provenance and peer review Not commissioned; externally peer reviewed.

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