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.
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.
Authors: Cristina Lamos; Charlotte Mihaljevic; Sebastian Aulmann; Thomas Bruckner; Christoph Domschke; Markus Wallwiener; Carmen Paringer; Herbert Fluhr; Sarah Schott; Christine Dinkic; Janina Brucker; Michael Golatta; Lisa Gensthaler; Michael Eichbaum; Christof Sohn; Joachim Rom Journal: PLoS One Date: 2016-12-01 Impact factor: 3.240
Authors: Ziena Abdulrahman; Noel de Miranda; Edith M G van Esch; Peggy J de Vos van Steenwijk; Hans W Nijman; Marij J P Welters; Mariette I E van Poelgeest; Sjoerd H van der Burg Journal: J Immunother Cancer Date: 2020-03 Impact factor: 13.751
Authors: Ziena Abdulrahman; Noel F C C de Miranda; Bart W J Hellebrekers; Peggy J de Vos van Steenwijk; Edith M G van Esch; Sjoerd H van der Burg; Mariette I E van Poelgeest Journal: Int J Cancer Date: 2020-07-03 Impact factor: 7.396
Authors: Erica R Heitmann; Kamani M Lankachandra; Jeff Wall; George D Harris; Hollie J McKinney; G Reza Jalali; Yogita Verma; Eric Kershnar; Michael W Kilpatrick; Petros Tsipouras; Diane M Harper Journal: PLoS One Date: 2012-07-06 Impact factor: 3.240