Abstract
Vulvar cancer is the fourth most common gynecological cancer worldwide. However, limited studies have been completed on the molecular characterization of vulvar squamous cell carcinoma resulting in a poor understanding of the disease initiation and progression. Analysis and early detection of the precursor lesion of HPV-independent vulvar squamous cell carcinoma (VSCC), differentiated vulvar intraepithelial neoplasia (dVIN), is of great importance given dVIN lesions have a high level of malignant potential. Here we present an examination of adjacent normal vulvar epithelium, dVIN, and VSCC from six patients by peptide Matrix-assisted laser desorption/ionization Mass Spectrometry Imaging (MALDI-MSI). The results reveal the differential expression of multiple peptides from the protein cytokeratin 5 (CK5) across the three vulvar tissue types. The difference observed in the relative abundance of CK5 by MALDI-MSI between the healthy epithelium, dVIN, and VSCC was further analyzed by immunohistochemistry (IHC) in tissue from eight VSCC patients. A decrease in CK5 immunostaining was observed in the VSCC compared to the healthy epithelium and dVIN. These results provide an insight into the molecular fingerprint of the vulvar intraepithelial neoplasia that appears to be more closely related to the healthy epithelium than the VSCC.
Highlights
Vulvar cancer is the fourth most common gynecological cancer worldwide, constituting 5% of all gynecological cancers and 0.6% of all cancer cases in women [1]
Mutations in the tumor suppressor gene TP16 are associated with human papilloma virus (HPV) related vulvar squamous cell carcinoma (VSCC), while mutations in TP53 have been shown to promote the development of non-HPV related VSCC from the inflammatory condition lichen sclerosus [2]
We present an examination of adjacent normal vulvar epithelium, differentiated vulvar intraepithelial neoplasia (dVIN), and VSCC from six patients by peptide MALDI-MSI
Summary
Vulvar cancer is the fourth most common gynecological cancer worldwide, constituting 5% of all gynecological cancers and 0.6% of all cancer cases in women [1]. The HPV related and non-HPV related forms of vulvar cancer have distinct precursor lesions, known as usual-type vulvar intraepithelial neoplasia and differentiated vulvar intraepithelial neoplasia, respectively. The incidence rates of non-HPV related invasive vulvar cancer and its precursor lesion, differentiated vulvar intraepithelial neoplasia (dVIN), have significantly increased amongst young women [3,4]. In Australia, the incidence rates of the disease are extremely high among Aboriginal women from Arnhem Land in the Northern Territory. Studies conducted within this cohort have found no relation between the disease and HPV infection or any underlying genomic irregularities that differentiate this group from other VSCC patients [3,4]
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