scholarly journals Differentiated vulvar intraepithelial neoplasia is often found in lesions, previously diagnosed as lichen sclerosus, which have progressed to vulvar squamous cell carcinoma

2010 ◽  
Vol 24 (2) ◽  
pp. 297-305 ◽  
Author(s):  
Hedwig P van de Nieuwenhof ◽  
Johan Bulten ◽  
Harrie Hollema ◽  
Rianne G Dommerholt ◽  
Leon F A G Massuger ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Lichen Sclerosus ◽  
Intraepithelial Neoplasia ◽  
Vulvar Intraepithelial Neoplasia ◽  
Vulvar Squamous Cell Carcinoma

scholarly journals Somatic Mutation Profiling in Premalignant Lesions of Vulvar Squamous Cell Carcinoma

2020 ◽  
Vol 21 (14) ◽  
pp. 4880 ◽  
Author(s):  
Sebastian Zięba ◽  
Anne-Floor W. Pouwer ◽  
Artur Kowalik ◽  
Kamil Zalewski ◽  
Natalia Rusetska ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Lichen Sclerosus ◽  
Intraepithelial Neoplasia ◽  
Genetic Alterations ◽  
Premalignant Lesions ◽  
Vulvar Intraepithelial Neoplasia ◽  
Vulvar Squamous Cell Carcinoma ◽  
Pathogenic Mutations

Vulvar squamous cell carcinoma (VSCC) originates from the progression of either a high-grade squamous intraepithelial lesion (HSIL) or differentiated-type vulvar intraepithelial neoplasia (dVIN), often in a background of lichen sclerosus (LS). The mechanisms leading to the progression of these premalignant lesions to VSCC are elusive. This study aims to identify pathogenic mutations implicated in VSCC development. Using next-generation sequencing, 38 HSIL, 19 dVIN, 20 LS, of which 10 were solitary lesions and 10 with adjacent VSCC, and 10 VSCC adjacent to LS, were screened for hotspot mutations in 50 genes covered by the Ion AmpliSeq Cancer Hotspot Panel v2 Kit (Thermo Fisher Scientific). Pathogenic mutations of TP53 were the most common genetic alterations identified in 53% and 24% of dVIN and HSIL cases, respectively, followed by CDKN2A (p16) mutated in 42% and 0% of dVIN and HSIL, respectively. Seven (70%) and three (30%) of 10 cases of VSCC associated with LS carried TP53 and CDKN2A mutations, respectively, whereas neither solitary LS nor LS associated with VSCC cases harbored mutations in these genes. It appears that TP53 mutations are early events during VSCC carcinogenesis, being present in both HSIL and dVIN lesions. Our preliminary data do not support a genetic background for the notion of LS as the VSCC premalignant lesion.

scholarly journals Vulvar intraepithelial neoplasia: Incidence and long‐term risk of vulvar squamous cell carcinoma

2020 ◽  
Vol 148 (1) ◽  
pp. 90-98 ◽  
Author(s):  
Nikki B. Thuijs ◽  
Marc Beurden ◽  
Annette H. Bruggink ◽  
Renske D. M. Steenbergen ◽  
Johannes Berkhof ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Intraepithelial Neoplasia ◽  
Vulvar Intraepithelial Neoplasia ◽  
Vulvar Squamous Cell Carcinoma

Clinical and molecular classification of vulvar squamous pre-cancers

2019 ◽  
Vol 29 (4) ◽  
pp. 821-828 ◽  
Author(s):  
Paul A Cohen ◽  
Lyndal Anderson ◽  
Lois Eva ◽  
James Scurry
Keyword(s):  
Squamous Cell Carcinoma ◽  
Next Generation Sequencing ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Intraepithelial Neoplasia ◽  
Vulvar Intraepithelial Neoplasia ◽  
Next Generation ◽  
Vulvar Squamous Cell Carcinoma ◽  
Increased Risk ◽  
Generation Sequencing

Vulvar intraepithelial neoplasia (VIN) is a precursor to vulvar squamous cell carcinoma and is defined histopathologically by the presence of atypia. VIN has been classified into two types: usual vulvar intraepithelial neoplasia (uVIN), which is also referred to as a vulvar high-grade squamous intra-epithelial lesion (HSIL), and differentiated VIN (dVIN). The former is associated with chronic infection by sub-types of the human papilloma virus (HPV), whereas dVIN is HPV-independent and frequently associated with lichen sclerosus. The distinction is important because dVIN has a greater risk of, and more rapid transit to, vulvar squamous cell carcinoma. Furthermore, dVIN-associated vulvar cancers have an increased risk of recurrence and higher mortality than those arising from HSIL. Molecular characterization of vulvar squamous cell carcinoma precursors using next-generation sequencing is a relatively novel, but rapidly advancing field. This review appraises recent studies that have investigated the risks of progression to vulvar malignancy associated with HSIL and dVIN, the prognosis of HPV-dependent and HPV-independent vulvar squamous cell carcinomas, and conducted next generation sequencing mutation analyses to elucidate the genomic profiles underlying VIN. These studies suggest that HSIL and dVIN are characterized by different underlying molecular alterations that may have important implications for treatment and follow-up of women diagnosed with vulvar squamous cell cancer.

scholarly journals Two Distinct Pathways to Development of Squamous Cell Carcinoma of the Vulva

2011 ◽  
Vol 2011 ◽  
pp. 1-7 ◽  
Author(s):  
Yutaka Ueda ◽  
Takayuki Enomoto ◽  
Toshihiro Kimura ◽  
Kiyoshi Yoshino ◽  
Masami Fujita ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Elderly Women ◽  
Malignant Tumors ◽  
Lichen Sclerosus ◽  
Intraepithelial Neoplasia ◽  
Genetic Alterations ◽  
Vulvar Intraepithelial Neoplasia ◽  
Hpv Dna

Squamous cell carcinoma (SCC) accounts for approximately 95% of the malignant tumors of the vaginal vulva and is mostly found in elderly women. The future numbers of patients with vulvar SCC is expected to rise, mainly because of the proportional increase in the average age of the general population. Two different pathways for vulvar SCC have been put forth. The first pathway is triggered by infection with a high-risk-type Human Papillomavirus (HPV). Integration of the HPV DNA into the host genome leads to the development of a typical vulvar intraepithelial neoplasia (VIN), accompanied with overexpression of and . This lesion subsequently forms a warty- or basaloid-type SCC. The HPV vaccine is a promising new tool for prevention of this HPV related SCC of the vulva. The second pathway is HPV-independent. Keratinizing SCC develops within a background of lichen sclerosus (LS) through a differentiated VIN. It has a different set of genetic alterations than those in the first pathway, including p53 mutations, allelic imbalances (AI), and microsatellite instability (MSI). Further clinical and basic research is still required to understand and prevent vulvar SCC.Capsule. Two pathway for pathogenesis of squamous cell carcinoma of the value are reviewed.

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