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

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...

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Veröffentlicht in:Experimental dermatology 2022-12, Vol.31 (12), p.1920-1926
Hauptverfasser: Gleue, Casey A., Xie, Fangyi, Deschaine, Maria, Dasari, Surendra, Sartori‐Valinotti, Julio C., Torgerson, Rochelle R., Davis, Mark D. P., Charlesworth, M. Cristine, Meves, Alexander, Lehman, Julia S.
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container_end_page 1926
container_issue 12
container_start_page 1920
container_title Experimental dermatology
container_volume 31
creator Gleue, Casey A.
Xie, Fangyi
Deschaine, Maria
Dasari, Surendra
Sartori‐Valinotti, Julio C.
Torgerson, Rochelle R.
Davis, Mark D. P.
Charlesworth, M. Cristine
Meves, Alexander
Lehman, Julia S.
description 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‐γ 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.
doi_str_mv 10.1111/exd.14660
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Interferon‐γ 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. 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subjects Calcium channels (voltage-gated)
Carcinogenesis
Carcinoma, Squamous Cell - metabolism
Cell Transformation, Neoplastic
Female
Genital diseases
Humans
lichen sclerosus
Malignancy
Mass spectroscopy
Proteomics
Risk factors
Squamous cell carcinoma
Therapeutic targets
Vulva
vulvar lichen sclerosus
Vulvar Lichen Sclerosus - complications
Vulvar Lichen Sclerosus - metabolism
Vulvar Lichen Sclerosus - pathology
Vulvar Neoplasms - pathology
vulvar squamous cell carcinoma
women's health
γ-Interferon
title Differential proteomic expression in indolent vulvar lichen sclerosus, transforming vulvar lichen sclerosus and normal vulvar tissue
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