Vulval squamous cell carcinoma and its precursors

Singh, Naveena; Gilks, C Blake

doi:10.1111/his.13989

Cited by 84 publications

(130 citation statements)

References 51 publications

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“…Because dVIN is often difficult to recognize for patients as well as for clinicians, including pathologists, it may partly explain why so few patients have been diagnosed with dVIN 23,25,26 . Signs of dVIN can be variable and often subtle, leading to misdiagnoses and inadequate clinical care due to diagnostic delay, especially in centers with limited exposure to this rare disease 27‐29 . It has been shown that dVIN was missed in 42% of biopsies initially diagnosed as LS in a series of patients who developed VSCC 30 .…”

Section: Discussionmentioning

confidence: 99%

Vulvar intraepithelial neoplasia: Incidence and long‐term risk of vulvar squamous cell carcinoma

Thuijs

Beurden

Bruggink³

et al. 2020

Intl Journal of Cancer

112

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The risk of vulvar squamous cell carcinoma (VSCC) in patients with high-grade vulvar intraepithelial neoplasia (VIN) is considered lower in high-grade squamous intraepithelial lesion (HSIL) compared to differentiated VIN (dVIN), but studies are limited. Our study investigated both the incidence of high-grade VIN and the cumulative incidence of VSCC in patients with HSIL and dVIN separately. A database of women diagnosed with highgrade VIN between 1991 and 2011 was constructed with data from the Dutch Pathology Registry (PALGA). The European standardized incidence rate (ESR) and VSCC risk were calculated, stratified for HSIL and dVIN. The effects of type of VIN (HSIL vs dVIN), age and lichen sclerosis (LS) were estimated by Cox regression. In total, 1148 patients were diagnosed with high-grade VIN between 1991 and 2011. Between 1991-1995 and 2006-2011, the ESR of HSIL increased from 2.39 (per 100 000 woman-years) to 3.26 and the ESR of dVIN increased from 0.02 to 0.08. The 10-year cumulative VSCC risk was 10.3%; 9.7% for HSIL and 50.0% for dVIN (log rank P < .001). Type of VIN, age and presence of LS were independent risk factors for progression to VSCC, with hazard ratios of 3.0 (95% confidence interval [CI] 1.3-7.1), 2.3 (95% CI 1.5-3.4) and 3.1 (95% CI 1.8-5.3), respectively. The incidence of high-grade VIN is rising. Because of the high cancer risk in patients with dVIN, better identification and timely recognition are urgently needed.

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Section: Discussionmentioning

confidence: 99%

Vulvar intraepithelial neoplasia: Incidence and long‐term risk of vulvar squamous cell carcinoma

Thuijs

Beurden

Bruggink³

et al. 2020

Intl Journal of Cancer

112

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“…The precursor lesion of VSCC is high‐grade vulvar intraepithelial neoplasia (VIN). VIN is classified into high‐grade squamous intraepithelial lesion (HSIL), which is human papillomavirus (HPV) related, and differentiated VIN (dVIN), which is independent of HPV and associated with lichen sclerosus 1‐3 . HSIL, previously known as usual type of VIN (uVIN), is the most common type of VIN, occurring mainly in women aged between 35 and 50 years.…”

Section: Introductionmentioning

confidence: 99%

DNA methylation markers for cancer risk prediction of vulvar intraepithelial neoplasia

Thuijs

Berkhof

Özer

et al. 2021

Intl Journal of Cancer

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Current clinical and histological classifications are unable to determine the risk of vulvar squamous cell carcinoma (VSCC) in high‐grade vulvar intraepithelial neoplasia (VIN), making prognostic biomarkers highly needed. We studied host‐cell DNA methylation markers in high‐grade squamous intraepithelial lesion (HSIL) and differentiated VIN (dVIN) without VSCC, in HSIL and dVIN adjacent to VSCC and in human papillomavirus (HPV) positive and negative VSCC, relative to control vulvar tissues. A series of 192 formalin‐fixed paraffin‐embedded vulvar samples, including VSCC (n = 58), VIN adjacent to VSCC (n = 30), VIN without VSCC during follow‐up (n = 41) and normal vulvar tissues (n = 63), were tested for 12 DNA methylation markers with quantitative multiplex methylation‐specific PCR (qMSP). HPV status was determined by p16INK4A immunohistochemistry and high‐risk HPV PCR analysis. Logistic regression analyses were used to determine methylation patterns and methylation marker performance for VIN and VSCC detection. Methylation markers showed significantly higher methylation levels with increasing severity of disease. VIN adjacent to VSCC showed a similar methylation‐high pattern as VSCC, while VIN without VSCC displayed a heterogeneous methylation pattern. Vulvar carcinogenesis is associated with increased DNA methylation. Higher DNA methylation levels in VIN seem to reflect higher cancer risk, emphasizing the high potential of DNA methylation biomarkers in the diagnostic workup of VIN. As a next step, longitudinal studies are needed to verify the prognostic value of methylation biomarkers as a clinical tool for stratification of cancer risk in women with VIN.

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“…To date, no other study had reported this phenomenon. Someone suggested that the morphological features of HPVindependent and HPV-associated precursor lesions can overlap, based on HE Staining [7]. Perhaps, it can be used to explain that phenomenon in our case report.…”

Section: Discussionmentioning

confidence: 59%

“…DVIN, VAAD and DE-VIL were belong to the precursor lesions of HPV-independent VSCC [7]. DE-VIL show prominent acanthosis and papillomatosis, but minimal atypia.…”

Section: Discussionmentioning

confidence: 94%

A Precursor to HPV-Independent VSCC : Differentiated Exophytic Vulvar Intraepithelial Lesion - A Case Report

Zheng

2020

Preprint

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Background: Vulvar cancer is a relatively rare gynecologic malignant disease. The majority of these tumors are vulvar squamous cell carcinoma (VSCC). There are two distinct aetiopathogenic pathways leading to VSCC: human papillomavirus (HPV)-dependent and HPV-independent. The precursor lesions of HPV-independent VSCC include differentiated vulvar intraepithelial neoplasia(VIN), vulvar acanthosis with altered differentiation(VAAD) and differentiated exophytic vulvar intraepithelial lesion(DE-VIL) . To date, the report of DE-VIL has not been found after this term was proposed in 2017. So it usually has been under-recognised by pathologists in the past owing to the incidence of DE-VIL is relatively small.Case presentation: Here, we report a typical case of DE-VIL, which exhibits the absence of HPV infection and mutations in TP53. Interesting, a small lesion showed similar morphologic feature to HSIL nearby the lesion of DE-VIL.However, it showed same immunochemical patterns with DE-VIL. To date, no other study has reported this phenomenon. Whether it is a rare subtype of DE-VIL or only a accompanying status is still unclear.Conclusions: As the precursor lesions of HPV-independent VSCC, DE-VIL was too difficult to diagnosis due to the lack of sufficient evidence. Therefore, we should pay more and more attention for DE-VIL.

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Vulval squamous cell carcinoma and its precursors

Cited by 84 publications

References 51 publications

Vulvar intraepithelial neoplasia: Incidence and long‐term risk of vulvar squamous cell carcinoma

Vulvar intraepithelial neoplasia: Incidence and long‐term risk of vulvar squamous cell carcinoma

DNA methylation markers for cancer risk prediction of vulvar intraepithelial neoplasia

A Precursor to HPV-Independent VSCC : Differentiated Exophytic Vulvar Intraepithelial Lesion - A Case Report

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Vulval squamous cell carcinoma and its precursors

Cited by 84 publications

References 51 publications

Vulvar intraepithelial neoplasia: Incidence and long‐term risk of vulvar squamous cell carcinoma

Vulvar intraepithelial neoplasia: Incidence and long‐term risk of vulvar squamous cell carcinoma

DNA methylation markers for cancer risk prediction of vulvar intraepithelial neoplasia

A Precursor to HPV-Independent VSCC&nbsp;: Differentiated Exophytic Vulvar Intraepithelial Lesion -&nbsp;A Case Report

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A Precursor to HPV-Independent VSCC : Differentiated Exophytic Vulvar Intraepithelial Lesion - A Case Report