Human Papillomavirus, Lichen Sclerosus, and Squamous Cell Carcinoma of the Vulva: Detection and Prognostic Significance

Ansink, Anca C.; Krul, M. R. L.; Weger, Roel A. de; Kleyne, J.; Pijpers, Helga W.; Tinteren, Harm van; Kraker, E. W. De; Helmerhorst, Th.J.M.; Heintz, A. Peter M.

doi:10.1006/gyno.1994.1028

Cited by 98 publications

(54 citation statements)

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“…However, the majority of vulvar squamous cell carcinoma patients do not have a recorded and histopathologically proven history of lichen sclerosus, but suffer from lichen sclerosus, either asymptomatic or unnoticed. 4,28,[31][32][33] This may result in delayed diagnosis by both patients and doctors. In our vulvar clinic, the policy is to biopsy every woman with a suspicion of lichen sclerosus, because this diagnosis has the consequence of a lifelong follow-up (at least yearly).…”

Section: Discussionmentioning

confidence: 99%

Differentiated vulvar intraepithelial neoplasia is often found in lesions, previously diagnosed as lichen sclerosus, which have progressed to vulvar squamous cell carcinoma

et al. 2011

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Lichen sclerosus is considered to be the precursor lesion of vulvar squamous cell carcinoma, of which only 2-5% progress to squamous cell carcinoma. Differentiated vulvar intraepithelial neoplasia (VIN) has been proposed to be the direct precursor lesion, but this is a recently recognized, and a difficult to diagnose, entity, which may easily be mistaken for a benign dermatosis. The aim of this study was to test the hypothesis that of all lesions that have been diagnosed as lichen sclerosus in the past, a part might currently be diagnosed as differentiated VIN, and to identify histopathological differences between lichen sclerosus lesions with and without progression to vulvar squamous cell carcinoma. All lichen sclerosus slides were revised by two expert gynecopathologists and histopathological characteristics were documented. After revision of lichen sclerosus biopsies without progression (n ¼ 61), 58 were reclassified as lichen sclerosus. Revision of lichen sclerosus biopsies with progression yielded concordant diagnoses in 18 of 60 cases (30%). Of 60 lesions, 25 (42%) were reclassified as differentiated VIN. The median time from differentiated VIN to vulvar squamous cell carcinoma was shorter (28 months) than that from lichen sclerosus to vulvar squamous cell carcinoma (84 months) (Po0.001). Lichen sclerosus that progressed to squamous cell carcinoma, but did not meet the criteria for differentiated VIN, more often showed parakeratosis (P ¼ 0.004), dyskeratosis (Po0.001), hyperplasia (P ¼ 0.048) and basal cellular atypia (P ¼ 0.009) compared with lichen sclerosus without progression. In conclusion, differentiated VIN diagnosis has been frequently missed and is associated with rapid progression to squamous cell carcinoma. Patients with lichen sclerosus with dyskeratosis and parakeratosis, hyperplasia and/or basal cellular atypia should be kept under close surveillance as these lesions also tend to progress to squamous cell carcinoma.

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Section: Discussionmentioning

confidence: 99%

Differentiated vulvar intraepithelial neoplasia is often found in lesions, previously diagnosed as lichen sclerosus, which have progressed to vulvar squamous cell carcinoma

et al. 2011

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“…However, another study failed to show a strong relationship between tumor subtype and HPV infection. 24 Additionally, Ansink et al 41 identified lichen sclerosus adjacent to about 37% of HPV-positive invasive squamous vulvar carcinomas in older women, and Madeleine et al reported an increased risk for invasive squamous vulvar carcinoma among women greater than 60 years of age when associated with HPV16 seropositivity and having more than two sexual partners. Perhaps HPV-associated invasive squamous vulvar carcinoma is increasing among the elderly, as it apparently is in younger women, [2][3][4] and is not as limited by histologic pattern as previously thought.…”

mentioning

confidence: 99%

Distribution of human papillomavirus genotypes in invasive squamous carcinoma of the vulva

et al. 2008

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Many studies have established a critical role for human papillomavirus (HPV) in the development of anogenital squamous neoplasia. In this report, we show the distribution of 37 high-and low-risk HPV types in 116 cases of invasive squamous vulvar carcinoma. Sections from paraffin-embedded tissue blocks were dissected as necessary to select areas of invasive carcinoma. Clinical and pathologic variables were analyzed using t-tests, univariate odds ratios and logistic regression analysis. Seventy percent of cases were HPV-positive, with an average patient age of 65 years (n ¼ 81). HPV-negative cases (n ¼ 35) had a higher average age (70 years), but these populations were not statistically different (t ¼ 1.65, P ¼ 0.10). HPV16 was most common (n ¼ 65). Other HPV types were less frequent (HPV33, n ¼ 12; HPV45, n ¼ 4; HPV52 and 6, each n ¼ 3; HPV18, 53 and 62, each n ¼ 2). Additional HPV types were identified only once. Multiple infections typically included HPV16 (12/14 cases). Tumors showing low-risk HPV (11 cases) and low-risk HPV only (three cases) were uncommon. Regional node metastasis was documented in 29 of 116 tumors, and 8/9 HPV-positive nodes contained HPV types identical to the primary tumor. Of tumor types, warty carcinoma was most strongly associated with highrisk HPV (odds ratio 4.34, 95% confidence interval 1.32-18.45), particularly high-risk HPVs other than type 16 (odds ratio 9.04, 95% confidence interval 1.60-54.00). Tumors associated with any HPV type (odds ratio 0.40, 95% confidence interval 0.14-1.17), any high-risk type (odds ratio 0.36, 95% confidence interval 0.12-1.08), or type 16 alone (odds ratio 0.34, 95% confidence interval 0.11-1.12) were less likely to metastasize than HPV-negative tumors. Correcting for possible confounding variables, such as patient age and tumor histology, linear logistic regression analysis confirmed this association (high-risk HPV odds ratio 0.28, 95% confidence interval 0.09-0.89).

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“…27,28 The frequency of regional nodal metastases varies with anatomic site, histologic features such as increasing tumor thickness and histologic dedifferentiation, tumor size, host immune competency, perineural invasion, and prior treatment. 19,[28][29][30][31][32][33][34][35] Squamous cell tumors arising in nonglabrous mucocutaneous sites such as the lip, vulva, penis, and perianal area are also more likely to metastasize than those involving other areas of the skin. 29 Squamous cell carcinoma arising in areas of chronic inflammation, nonhealing wounds, chronic osteomyelitis, and in irradiated fields are known to be particularly aggressive, with rates of nodal metastases between 18% and 30%.…”

Section: Commentmentioning

confidence: 99%

Sentinel Node Biopsy for High-Risk Nonmelanoma Cutaneous Malignancy

Wagner

Evdokimow²,

Weisberger³

et al. 2004

Arch Dermatol

109

102

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Human Papillomavirus, Lichen Sclerosus, and Squamous Cell Carcinoma of the Vulva: Detection and Prognostic Significance

Cited by 98 publications

References 0 publications

Differentiated vulvar intraepithelial neoplasia is often found in lesions, previously diagnosed as lichen sclerosus, which have progressed to vulvar squamous cell carcinoma

Differentiated vulvar intraepithelial neoplasia is often found in lesions, previously diagnosed as lichen sclerosus, which have progressed to vulvar squamous cell carcinoma

Distribution of human papillomavirus genotypes in invasive squamous carcinoma of the vulva

Sentinel Node Biopsy for High-Risk Nonmelanoma Cutaneous Malignancy

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