scholarly journals Vulvar Diseases that Required a Biopsy: A Retrospective Study

2021 ◽  
Vol 79 (4) ◽  
pp. 321-328
Author(s):  
Rita Bouceiro-Mendes ◽  
M. Mendonça-Sanches ◽  
Luís Soares-de-Almeida ◽  
Isabel Correia-Fonseca ◽  
João Borges-da-Costa
Keyword(s):  
Squamous Cell Carcinoma ◽  
Retrospective Study ◽  
Lichen Sclerosus ◽  
Intraepithelial Neoplasia ◽  
Vulvar Intraepithelial Neoplasia ◽  
Central Hospital ◽  
Clinical Appearance ◽  
Vulvar Diseases ◽  
Histological Confirmation ◽  
Correct Understanding

Introduction: The vulvar area may be affected by many noninfectious conditions with similar clinical appearance, requiring a cutaneous biopsy. Our goal was to characterize the noninfectious vulvar diseases that required a biopsy in a southwestern Europe Central Hospital during a 10-year period. Methods: A retrospective study of all the noninfectious vulvar diseases with histological confirmation diagnosed in our institution was conducted between January 1, 2008 and December 31, 2017. Results: The sample included a total of 323 biopsies from 317 patients, aged between 11 and 98 years (mean age of 54.2 years). A total of 36 vulvar diseases was identified. Neoplastic conditions were the most frequently found, particularly melanotic macules (22.3%). The most frequent malignant tumor was vulvar intraepithelial neoplasia (6.2%) and squamous cell carcinoma (5.6%). The most common dermatosis was lichen sclerosus (12.7%). Conclusion: Neoplasms were the most frequently diagnosed conditions affecting the vulvar area that required a biopsy. Ruling out malignancy was also the main reason to perform a biopsy. This study highlights the variety of noninfectious diseases that may affect the vulva and require a biopsy. Since vulvar diseases may be serious and carry high levels of patient distress a correct understanding of these conditions is crucial.

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.

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.

HPV-related Vulvar Diseases and Perspectives of p16INK4a Immunochemistry: A Review of the Literature

2017 ◽  
Vol 103 (6) ◽  
pp. 511-515 ◽  
Author(s):  
Angela Carrone ◽  
Lucia Riganelli ◽  
Delia Savone ◽  
Assunta Casorelli ◽  
Lucia Merlino ◽  
...  
Keyword(s):  
Lichen Sclerosus ◽  
Intraepithelial Neoplasia ◽  
Hpv Infection ◽  
Vulvar Intraepithelial Neoplasia ◽  
Cochrane Library ◽  
Management Options ◽  
Related Disease ◽  
Associated Lesions ◽  
Online Databases ◽  
P53 Immunoreactivity

Introduction Two different types of vulvar intraepithelial neoplasia (VIN), HPV-related and HPV-unrelated, should be considered as two separate entities with different management options. The incidence of HPV-related VIN is increasing worldwide and is implicated in carcinogenesis. Our objective is to investigate the use of p16INK4a immunostaining or p16INK4a/p53 double staining for the detection of HPV-related disease to overcome the problem that histological criteria often have significant overlap. Methods A systematic literature search was carried out in the online databases PubMed, EMBASE, Cochrane Library, Clincaltrials.gov and Scopus. The key search terms were HPV, VIN, p16INK4a immunochemistry and p53. Results We found that nuclear and cytoplasmic immunostaining for p16INK4a was intense and diffuse in HPV-associated lesions and weak and focal in normal vulvar epithelium, nondysplastic lesions, lichen sclerosus and keratinizing vulvar squamous cell carcinoma. p53 nuclear immunostaining was always negative in HPV-related disease. Conclusions Our findings indicated that p16INK4a or p16INK4a/p53 immunoreactivity, along with histological diagnosis, could be a convenient means to adequately classify VIN and its connection to HPV infection. Therefore, the clear recognition of HPV-associated VIN would lead to an appropriate strategy of treatment and follow-up.

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.

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