Immunohistochemical Expression of SOX2 in Vulvar Intraepithelial Neoplasia and Squamous Cell Carcinoma

2013 ◽  
Vol 32 (3) ◽  
pp. 323-328 ◽  
Author(s):  
Hermann Brustmann ◽  
Andreas Brunner
Keyword(s):  
Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Intraepithelial Neoplasia ◽  
Vulvar Intraepithelial Neoplasia ◽  
Immunohistochemical Expression

Immunohistochemical expression of p16 and p53 in vulvar intraepithelial neoplasia and squamous cell carcinoma of the vulva

2006 ◽  
Vol 12 (3) ◽  
pp. 153-157 ◽  
Author(s):  
Mauricio Cordoni Nogueira ◽  
Ernesto de Paula Guedes Neto ◽  
Marcos Wengrover Rosa ◽  
Eduardo Zettler ◽  
Cláudio Galleano Zettler
Keyword(s):  
Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Intraepithelial Neoplasia ◽  
Vulvar Intraepithelial Neoplasia ◽  
Immunohistochemical Expression

scholarly journals Expression of Human Telomerase Reverse Transcriptase in Vulvar Intraepithelial Neoplasia and Squamous Cell Carcinoma: An Immunohistochemical Study With Survivin and p53

2012 ◽  
Vol 136 (11) ◽  
pp. 1359-1365 ◽  
Author(s):  
Alfred Wellenhofer ◽  
Hermann Brustmann
Keyword(s):  
Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Intraepithelial Neoplasia ◽  
Vulvar Intraepithelial Neoplasia ◽  
Telomerase Reverse Transcriptase ◽  
High Grade ◽  
Human Telomerase Reverse Transcriptase ◽  
Keratinizing Squamous Cell Carcinoma ◽  
Human Telomerase

Context.—Human telomerase reverse transcriptase (hTERT), an enzyme that enables cells to overcome replicative senescence and to divide indefinitely, is overexpressed in many cancers and their precursor lesions. Objective.—To test whether hTERT expression is related to neoplastic progression and resistance to apoptosis in vulvar epithelia. Design.—Immunoexpression of hTERT was evaluated in 101 formalin-fixed, paraffin-embedded archival vulvar epithelia consisting of normal squamous vulvar epithelia (n  =  25), lichen sclerosus (n  =  10), high-grade classic vulvar intraepithelial neoplasia (n  =  16), differentiated vulvar intraepithelial neoplasia (n  =  18), and vulvar invasive keratinizing squamous cell carcinoma (n  =  32) and related to survivin and p53 expression. Immunostaining for all factors was scored for moderate and strong intensities with regard to quantity to determine upregulation and overexpression (score 0, 0% immunoreactive cells; score 1+, <5% immunoreactive cells; score 2+, 5% to 50% immunoreactive cells; score 3+, >50% immunoreactive cells). Score 3+ was considered as overexpression. Results.—Nuclear hTERT immunoexpression was closely related to survivin reactivity, increased from normal vulvar squamous epithelia to lichen sclerosus and to high-grade classic vulvar intraepithelial neoplasia, differentiated vulvar intraepithelial neoplasia, and invasive keratinizing squamous cell carcinoma (P < .001), and followed the morphologic distribution of atypical squamous epithelial cells. Overexpression of hTERT was comparable to that seen for p53 in invasive keratinizing squamous cell carcinoma (P  =  .62); significant differences were calculated for differentiated vulvar intraepithelial neoplasia (P  =  .003) and high-grade classic vulvar intraepithelial neoplasia (P  =  .001). Conclusion.—Human telomerase reverse transcriptase is upregulated in vulvar intraepithelial neoplasia and invasive keratinizing squamous cell carcinoma compared with nonneoplastic squamous epithelia of the vulva as an apparently early and preinvasive event in the neoplastic transformation, with development of cellular longevity and resistance to apoptosis by survivin activation as associated features, independent of the etiology of vulvar intraepithelial neoplasia.

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.

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