Trends in incidence and survival of Dutch women with vulvar squamous cell carcinoma

Schuurman, M.S.; Einden, L.C.G. van den; Massuger, Leon F.A.G.; Kiemeney, Lambertus A.; Aa, M.A. van der; Hullu, Joanne A. de

doi:10.1016/j.ejca.2013.08.003

Cited by 120 publications

(100 citation statements)

References 33 publications

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“…In the Netherlands, the incidence rate of vulvar cancer increased from 2.2 in 1990 to 3.4 per 100,000 woman-years in 2014 (3). Vulvar squamous cell carcinoma (VSCC) accounts for about 90% of all vulvar cancers (4). Although the etiology of VSCC is not yet fully understood, it is recognized to be heterogeneous.…”

Section: Introductionmentioning

confidence: 99%

Lichen Sclerosus: Incidence and Risk of Vulvar Squamous Cell Carcinoma

Bleeker

Visser²,

Overbeek³

et al. 2016

Cancer Epidemiology, Biomarkers &Amp; Prevention

204

157

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Background: The association between lichen sclerosus and vulvar squamous cell carcinoma (VSCC) has long been recognized, but large epidemiologic studies are lacking.Methods: Data of women diagnosed with vulvar pathology in the Netherlands were retrieved from the Dutch Pathology Registry. All vulvar pathology reports of this historical cohort were reviewed to construct a research database, including 3,038 women with lichen sclerosus diagnosed between 1991 and 2011. The incidence rate of lichen sclerosus and the cumulative incidence of VSCC among women with lichen sclerosus were estimated.Results: Between 1991 and 2011, the incidence rate of lichen sclerosus increased from 7.4 to 14.6 per 100,000 woman-years. The median age at time of lichen sclerosus diagnosis was 59.8 years and the cumulative VSCC incidence was 6.7%. The 10-year VSCC incidence in women with lichen sclerosus was associated

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Section: Introductionmentioning

confidence: 99%

Lichen Sclerosus: Incidence and Risk of Vulvar Squamous Cell Carcinoma

Bleeker

Visser²,

Overbeek³

et al. 2016

Cancer Epidemiology, Biomarkers &Amp; Prevention

204

157

View full text Add to dashboard Cite

show abstract

“…The mean age at diagnosis is about 70 years, and recent studies show that the increase in incidence rate is most pronounced in the oldest patient group (>80 years) [3]. Other studies, however, showed that the increase in incidence was especially attributable to the younger patients, and that this might be caused by an increase in premalignant human papillomavirus (HPV)-associated vulvar disease [4]. Squamous cell cancer of the vulva spreads by three routes: the initial metastatic spread occurs usually to the inguinofemoral lymph nodes.…”

Section: Vulvar Cancermentioning

confidence: 95%

Sentinel node biopsy in vulvar cancer: Implications for staging

Oonk

Hollema

Zee

2015

Best Practice & Research Clinical Obstetrics & Gynaecol

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“…Radical surgery has been the standard treatment for most patients but is accompanied by physical and psychological adverse effects and a considerable morbidity 1, 4. Less radical treatments have been introduced in the last two decades, yet with no significant improvements in survival 5. Therefore, identification of new biomarkers, those can predict tumor behavior, could be important for the development of better treatment strategies.…”

Section: Introductionmentioning

confidence: 99%

Evaluation of CHK1 activation in vulvar squamous cell carcinoma and its potential as a therapeutic target in vitro

et al. 2018

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CHK1 is an important regulator of the cell cycle and DNA damage response, and its altered expression has been identified in various tumors. Chk1 inhibitors are currently being evaluated as monotherapy and as potentiators of chemotherapy in clinical settings. However, to our knowledge, no previous study has investigated either the activation status or the therapeutic potential of CHK1 targeting in vulvar cancer. Therefore, we examined the expression status of activated CHK1 forms pCHK1Ser345, pCHK1Ser317, pCHK1Ser296, and pCHK1Ser280 in 294 vulvar squamous cell carcinomas (VSCC) using immunohistochemistry and analyzed their relationships with various clinicopathological variables and clinical outcome. To aid translation of preclinical studies, we also assessed cell sensitivity to the Chk1 inhibition in two vulvar cancer cell lines. Compared to the levels of pCHK1Ser345, pCHK1Ser317, pCHK1Ser296, and pCHK1Ser280 in normal vulvar squamous epithelium, high nuclear pCHK1Ser345 expression was found in 57% of vulvar carcinomas, whereas low nuclear pCHK1Ser317, pCHK1Ser296, and pCHK1Ser280 expressions were observed in 58%, 64%, and 40% of the cases, respectively. Low levels of pCHK1Ser317 and pCHK1Ser280 in the nucleus correlated significantly with advanced tumor behaviors and aggressive features. None of pCHK1Ser345, pCHK1Ser317, pCHK1Ser296, and pCHK1Ser280 forms were identified as prognostic factors. In vitro inhibition of CHK1 by small molecular inhibitors or siRNA reduced viability by inducing DNA damage and apoptosis of vulvar cancer cell lines. In summary, we conclude that cellular functions regulated by CHK1 are phosphorylation/localization‐dependent and deregulation of CHK1 function occurs in VSCC and might contribute to tumorigenesis. Targeting CHK1 might represent as a useful antitumor strategy for the subgroup of VSCC harboring p53 mutations.

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Trends in incidence and survival of Dutch women with vulvar squamous cell carcinoma

Cited by 120 publications

References 33 publications

Lichen Sclerosus: Incidence and Risk of Vulvar Squamous Cell Carcinoma

Lichen Sclerosus: Incidence and Risk of Vulvar Squamous Cell Carcinoma

Sentinel node biopsy in vulvar cancer: Implications for staging

Evaluation of CHK1 activation in vulvar squamous cell carcinoma and its potential as a therapeutic target in vitro

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