Human Papillomavirus DNA in Multicentric Vulvar Intraepithelial Neoplasia

Beurden, Marc van; Kate, F. W. Ten; Tjong-A-Hung, Steven P.; Craen, Anton Jm de; Vange, N. van der; Lammes, F. B.; Schegget, Jan ter

doi:10.1097/00004347-199801000-00003

Cited by 37 publications

(14 citation statements)

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“…The HPV type was not the same in just over 20% of the different lesions even if the biopsies were taken at the same time. 38,42 These findings suggest that multifocal disease is an HPV-related condition, and therefore in cases of multifocal VIN, a thorough examination of the entire lower female genital tract is recommended.…”

Section: Multifocal and Multicentric Diseasementioning

confidence: 99%

Squamous Vulvar Intraepithelial Neoplasia

Preti¹,

Seters²,

Sideri³

et al. 2005

Clinical Obstetrics and Gynecology

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Section: Multifocal and Multicentric Diseasementioning

confidence: 99%

Squamous Vulvar Intraepithelial Neoplasia

Preti¹,

Seters²,

Sideri³

et al. 2005

Clinical Obstetrics and Gynecology

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“…Physician sampling missed the diagnosis of genital high-risk HPV infection in 18.5% of women. This could reflect the multicentricity of HPV infection and the collection of HPVinfected cells from external genital sites [38]. Cervical swab specimens were collected after self-sampling and after a Papanicolaou smear was performed, which could have reduced the number of cells available for HPV detection.…”

Section: Notementioning

confidence: 99%

Self-Sampling Is Associated with Increased Detection of Human Papillomavirus DNA in the Genital Tract of HIV-Seropositive Women

Petignat¹,

Hankins²,

Walmsley

et al. 2005

Clinical Infectious Diseases

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“…23 In a third study, 93% of 27 patients had true multifocal disease but no correlation with invasion was performed. 24 If true multifocal VIN is as common as these last 2 studies suggest, then it is the norm rather than the exception. Given that our data suggest 2 possible aetiologies in multifocal VIN (separate clonal proliferations vs. epithelial spread of a single clonal proliferation), performing clonality assays may prove to be useful in predicting which women may develop invasive disease.…”

Section: Discussionmentioning

confidence: 99%

Molecular evidence of a common clonal origin and subsequent divergent clonal evolution in vulval intraepithelial neoplasia, vulval squamous cell carcinoma and lymph node metastases

Rosenthal

Ryan

Hopster

et al. 2002

Intl Journal of Cancer

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VIN is thought to be the precursor of some VSCCs because it is monoclonal, frequently occurs contiguously with VSCC and shares similar risk factors with a subgroup of VSCC. There has been no conclusive molecular evidence supporting this assumption. We performed X-chromosome inactivation analysis on 9 cases of lone VIN, 10 cases of VSCC and associated contiguous VIN and 11 cases of VSCC and associated noncontiguous VIN. Eight of the 9 cases of lone VIN appeared to be monoclonal. All 7 informative and monoclonal cases of VIN with contiguous VSCC and 6/9 informative cases of VIN with noncontiguous VSCC showed patterns of X-chromosome inactivation consistent with a common monoclonal origin for both VIN and VSCC. Two of the 9 cases of VIN with noncontiguous VSCC showed X-chromosome inactivation patterns consistent with a separate clonal origin. We performed LOH analysis at 6 chromosomal loci on these samples and 7 cases with lymph node metastases. Identical losses occurred 7 times in VIN and contiguous VSCC (random probability 1.2 ؋ 10 -9 ), twice in VIN and noncontiguous VSCC (random probability 1.5 ؋ 10 -3 ) and 3 times in VSCC and associated metastases (random probability 1.8 ؋ 10 -5 ). Some losses occurring in VSCC did not appear in the contiguous VIN or associated metastases and vice versa. These data provide molecular evidence that VIN is the precursor of VIN-associated VSCC, that multifocal disease may arise via either different clones or a single clone and that continued divergent clonal evolution may occur in vulval neoplasia. © 2002 Wiley-Liss, Inc. Key words: vulval intraepithelial neoplasia; vulval cancer; loss of heterozygosity; X-chromosome inactivation; vulval squamous cell carcinomaVIN has long been thought to be a premalignant condition that may progress to invasive VSCC. This assumption is based on observations that VIN frequently occurs contiguously with VSCC, 1 that VIN and a subgroup of VSCC are associated with similar risk factors (smoking, 2 immunosuppression 3 and HPV infection 2,4 ) and that VIN and VSCC are monoclonal neoplastic conditions. 5,6 Confirmation of this hypothesis is important for gaining insight into the process of vulval carcinogenesis. Furthermore, identifying molecular markers for risk of progression of VIN to VSCC is possible only if molecular evidence is compatible with a common monoclonal origin of the 2 conditions. We first wanted to confirm that VIN is a monoclonal condition. We then wanted to document the patterns of LOH events and X-chromosome inactivation in VSCC samples and contiguous and noncontiguous VIN, to examine whether VIN and VSCC could have arisen from the same clone. Because we had already studied the frequency of LOH at 6 chromosomal loci in lone VIN and VSCC, 7 it was possible to calculate the odds of identical losses occurring by chance in both VSCC and associated VIN. Finally, as primary cancers and their metastases are thought to have the same clonal origin, we compared the number of identical losses occurring in primaries and their metastases with the...

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Human Papillomavirus DNA in Multicentric Vulvar Intraepithelial Neoplasia

Cited by 37 publications

References 0 publications

Squamous Vulvar Intraepithelial Neoplasia

Squamous Vulvar Intraepithelial Neoplasia

Self-Sampling Is Associated with Increased Detection of Human Papillomavirus DNA in the Genital Tract of HIV-Seropositive Women

Molecular evidence of a common clonal origin and subsequent divergent clonal evolution in vulval intraepithelial neoplasia, vulval squamous cell carcinoma and lymph node metastases

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