scholarly journals Differentiated Vulvar Intraepithelial Neoplasia-like and Lichen Sclerosus-like Lesions in HPV-associated Squamous Cell Carcinomas of the Vulva

2018 ◽  
Vol 42 (6) ◽  
pp. 828-835 ◽  
Author(s):  
Natalia Rakislova ◽  
Laia Alemany ◽  
Omar Clavero ◽  
Marta del Pino ◽  
Adela Saco ◽  
...  
Keyword(s):  
Squamous Cell ◽  
Lichen Sclerosus ◽  
Intraepithelial Neoplasia ◽  
Squamous Cell Carcinomas ◽  
Vulvar Intraepithelial Neoplasia

Downregulated CD44 and hyaluronan expression in vulvar intraepithelial neoplasia and squamous cell carcinomas

2010 ◽  
Vol 89 (1) ◽  
pp. 108-119 ◽  
Author(s):  
Kirsi Hämäläinen ◽  
Veli-Matti Kosma ◽  
Marja-Liisa Eloranta ◽  
Raija Tammi ◽  
Markku Tammi ◽  
...  
Keyword(s):  
Squamous Cell ◽  
Intraepithelial Neoplasia ◽  
Squamous Cell Carcinomas ◽  
Vulvar Intraepithelial Neoplasia

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.

Continuous Spatial Sequences of Lichen Sclerosus, Penile Intraepithelial Neoplasia, and Invasive Carcinomas: A Study of 109 Cases

2019 ◽  
Vol 27 (5) ◽  
pp. 477-482 ◽  
Author(s):  
Sofía Cañete-Portillo ◽  
Diego F. Sanchez ◽  
María José Fernández-Nestosa ◽  
Adriano Piris ◽  
Patricia Zarza ◽  
...  
Keyword(s):  
Squamous Cell ◽  
Invasive Carcinoma ◽  
Precancerous Lesion ◽  
Spatial Relationship ◽  
Lichen Sclerosus ◽  
Intraepithelial Neoplasia ◽  
Squamous Cell Carcinomas ◽  
World Health ◽  
Invasive Carcinomas ◽  
Penile Intraepithelial Neoplasia

Lichen sclerosus (LSc) with penile cancer is found in about two thirds of specimens. It has been hypothesized that LSc represents a precancerous condition. To qualify as such, in addition to cytological atypia and similarity with the invasive tumor, a spatial correlation between LSc and neoplastic lesions needs to be demonstrated. The purpose of this study was to evaluate such a spatial relationship. Circumcision (28 cases) and penectomy (81 cases) specimens were evaluated. All cases had LSc, penile intraepithelial neoplasia (PeIN), and/or invasive squamous cell carcinomas. We examined LSc in relation to invasive carcinoma, PeIN, and normal epithelia. Invasive squamous cell carcinomas, classified according to the World Health Organization criteria as non–human papillomavirus (HPV)-related and HPV-related PeIN, were present in 100 cases. Non-HPV-related (differentiated) PeIN was the most common subtype associated with LSc (89%). There were 5 spatial patterns identified: (1) LSc adjacent to PeIN (23%), (2) LSc adjacent and comprising PeIN (42%), (3) LSc next to and within invasive carcinomas (8%), (4) LSc throughout the sequence PeIN-invasive carcinoma (24%), and (5) LSc was separate (with normal tissue between the lesions) from PeIN and/or invasive carcinomas in a minority of cases (3%). LSc within the cancer was not previously described. In this series, we found 35 cases with LSc within invasive carcinomas. The striking continuous spatial relationship among LSc, PeIN, and/or invasive carcinoma as shown in this study may be a necessary (but not sufficient) condition for the hypothesis postulating LSc as a penile precancerous lesion.

Gains of chromosome region 3q26 in intraepithelial neoplasia and invasive squamous cell carcinoma of the vulva are frequent and independent of HPV status

2008 ◽  
Vol 61 (9) ◽  
pp. 1034-1037 ◽  
Author(s):  
S Aulmann ◽  
J Schleibaum ◽  
R Penzel ◽  
P Schirmacher ◽  
G Gebauer ◽  
...  
Keyword(s):  
Squamous Cell ◽  
P53 Protein ◽  
In Situ Hybridisation ◽  
Intraepithelial Neoplasia ◽  
Squamous Cell Carcinomas ◽  
Invasive Squamous Cell Carcinoma ◽  
Fluorescence In Situ Hybridisation ◽  
P53 Expression ◽  
Usual Type ◽  
Hpv Status

Aims:Two different forms of vulvar intraepithelial neoplasia (VIN) are recognised: (1) usual-type (bowenoid) VIN, which is related to high-risk papillomavirus infection, and (2) differentiated (simplex) VIN, which is associated with chronic inflammation. The aim of this study was to investigate the presence of chromosome 3q26 gains in the spectrum of precancerous lesions and invasive squamous cell carcinomas (SCCs) of the vulva.Methods:3q26 gains were analysed using fluorescence in situ hybridisation in a series of usual-type VINs, VINs of the differentiated type and invasive squamous cell carcinomas. In addition, all cases were examined for human papillomavirus (HPV) DNA, p53 mutations, and p16 and p53 protein expression.Results:Gains of chromosome 3q26 were present in all VINs of the differentiated type and in 50% of the usual-type VIN lesions. 81% of SCCs were positive for 3q26 gains irrespective of the HPV status and of the associated precursor lesion. HPV-associated lesions exhibited the typical, strong cytoplasmic p16 accumulation while mutated p53 was only detected in HPV-negative VINs or SCCs, and was associated with an overexpression of p53 protein.Conclusions:Immunohistochemical evaluation of p16 and p53 expression aids in the differential diagnosis of squamous cell alterations of the vulva. However, detection of 3q26 imbalance is of additional diagnostic value in difficult cases of HPV-unrelated usual-type VINs and VINs of the differentiated type.

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