ArticleBritish journal of cancer2002
Genetic aberrations detected by comparative genomic hybridisation in vulvar cancers.
Article in British journal of cancer, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 47 citations in OpenAlex.
- Molecular events in the pathogenesis of vulvar squamous cell carcinoma.Seminars in diagnostic pathology · 2021Review
- Molecular heterogeneity in human papillomavirus-dependent and -independent vulvar carcinogenesis.Cancer medicine · 2018Article
- Article
- The economic burden of human papillomavirus-related precancers and cancers in Sweden.PloS one · 2017Article
- ROCK1 as a novel prognostic marker in vulvar cancer.BMC cancer · 2014Article
- High-resolution genomic profiling of human papillomavirus-associated vulval neoplasia.British journal of cancer · 2010Article
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Authors and funding
8 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Squamous cell carcinoma of the vulva is a disease of significant clinical importance, which arises in the presence or absence of human papillomavirus. We used comparative genomic hybridisation to document non-random chromosomal gains and losses within human papillomavirus positive and negative vulvar cancers. Gain of 3q was significantly more common in human papillomavirus-positive cancers compared to human papillomavirus-negative cancers. The smallest area of gain was 3q22-25, a chromosome region which is frequently gained in other human papillomavirus-related cancers. Chromosome 8q was more commonly gained in human papillomavirus-negative compared to human papillomavirus-positive cancers. 8q21 was the smallest region of gain, which has been identified in other, non-human papillomavirus-related cancers. Chromosome arms 3p and 11q were lost in both categories of vulvar cancer. This study has demonstrated chromosome locations important in the development of vulvar squamous cell carcinoma. Additionally, taken together with previous studies of human papillomavirus-positive cancers of other anogenital sites, the data indicate that one or more oncogenes important in the development and progression of human papillomavirus-induced carcinomas are located on 3q. The different genetic changes seen in human papillomavirus-positive and negative vulvar squamous cell carcinomas support the clinicopathological data indicating that these are different cancer types.
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