4.6 Article

Differential proteomic expression in indolent vulvar lichen sclerosus, transforming vulvar lichen sclerosus and normal vulvar tissue

Journal

EXPERIMENTAL DERMATOLOGY
Volume 31, Issue 12, Pages 1920-1926

Publisher

WILEY
DOI: 10.1111/exd.14660

Keywords

carcinogenesis; lichen sclerosus; proteomics; squamous cell carcinoma; vulvar lichen sclerosus; vulvar squamous cell carcinoma; women's health

Categories

Funding

  1. British Association of Dermatologists Geoffrey Dowling Fellowship
  2. The Appignani Lichen Planus Benefactor Gift at Mayo Clinic

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The study identified significant differences in protein expression between transforming VLS and indolent VLS, particularly in pathways related to cancer development. The results support the notion that VLS is a risk factor for VSCC and suggest potential biomarkers and therapeutic targets for future research.
Vulvar lichen sclerosus (VLS) confers approximately 3% risk of malignant transformation to vulvar squamous cell carcinoma (VSCC). We used unbiased proteomic methods to identify differentially expressed proteins in tissue of patients with VLS who developed VSCC compared to those who did not. We used laser capture microdissection- and nanoLC-tandem mass spectrometry to assess protein expression in individuals in normal vulvar tissue (NVT, n = 4), indolent VLS (no VSCC after at least 5 years follow-up, n = 5) or transforming VSCC (preceding VSCC, n = 5). Interferon-gamma and antigen-presenting pathways are overexpressed in indolent and transforming VLS compared to NVT. There was differential expression of malignancy-related proteins in transforming VLS compared to indolent VLS (CAV1 overexpression, AKAP12 underexpression), particularly in the EIF2 translation pathway, which has been previously implicated in carcinogenesis. Results of this study provide additional molecular evidence supporting the concept that VLS is a risk factor for VSCC and highlights possible future biomarkers and/or therapeutic targets.

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