Vulvar acanthosis with altered differentiation: is this entity a variant of hypertrophic lichen sclerosus?

Walton, Douglas B.; Stearns, Laurel; Fillman, Eric P.; Banks, Nancy; Dalton, Scott R.

doi:10.1111/cup.12557

Cited by 10 publications

(6 citation statements)

References 4 publications

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“…39 There were two subsequent case reports of VAAD; in one, the patient did have an associated verrucous carcinoma, and this progressed to conventional VSCC and eventually anaplastic carcinoma, resulting in the death of the patient, 49 whereas, in the other report, the authors questioned whether VAAD was a form of hyperplastic lichen sclerosus. 50 There were seven cases of VAAD in the molecular study of Nooij et al, and they confirmed that mutations in genes associated with VSCC could be found in some, including a TP53 mutation in one. 37 They did not, however, identify PIK3CA mutations in any of their cases, in contrast to the findings of Watkins et al 39 A B C D Figure 7.…”

Section: Differentiated Exophytic Vulvar Intraepithelial Lesionmentioning

confidence: 78%

“…These same authors, recognising the overlapping histological features with DEVIL, included VAAD as a form of DEVIL in their later study . There were two subsequent case reports of VAAD; in one, the patient did have an associated verrucous carcinoma, and this progressed to conventional VSCC and eventually anaplastic carcinoma, resulting in the death of the patient, whereas, in the other report, the authors questioned whether VAAD was a form of hyperplastic lichen sclerosus . There were seven cases of VAAD in the molecular study of Nooij et al ., and they confirmed that mutations in genes associated with VSCC could be found in some, including a TP53 mutation in one .…”

Section: Precursor Lesions Of Vsccmentioning

confidence: 99%

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Vulval squamous cell carcinoma and its precursors

2019

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Vulval squamous cell carcinoma (VSCC) can arise through two distinct pathways [human papillomavirus (HPV)‐associated and HPV‐independent], and these VSCC variants are recognised as different disease entities on the basis of different aetiologies, morphological features, molecular events during oncogenesis, precursor lesions, prognosis, and response to treatment. The precursor of HPV‐associated VSCC, variously referred to as high‐grade squamous intraepithelial lesion (HSIL) [vulvar intraepithelial neoplasia (VIN) 2/3] or usual‐type VIN, is morphologically identical to the more common HSIL (cervical intraepithelial neoplasia 2/3) of the cervix. The precursor lesions of HPV‐independent VSCC include differentiated VIN, differentiated exophytic vulvar intraepithelial lesion, and vulvar acanthosis with altered differentiation; these have been under‐recognised by pathologists in the past, leading to delays in treatment. This review will discuss the recent advances in diagnostic surgical pathology of VSCC and its precursors, and how these diagnoses can impact on patient management.

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Section: Differentiated Exophytic Vulvar Intraepithelial Lesionmentioning

confidence: 78%

Section: Precursor Lesions Of Vsccmentioning

confidence: 99%

Vulval squamous cell carcinoma and its precursors

2019

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“…114 Only two other reports of VAAD have been published in the literature since 2004, and both question whether VAAD is truly a distinct entity or whether it represents a morphological variant of hypertrophic LS or dVIN. 116,117 Further studies are needed to answer these questions.…”

Section: Diagnostic Challenges and Differential Diagnosismentioning

confidence: 99%

Squamous precursor lesions of the vulva: current classification and diagnostic challenges

et al. 2016

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Summary Growing evidence has established two major types of vulvar intraepithelial neoplasia (VIN), which correspond to two distinct oncogenic pathways to vulvar squamous cell carcinoma (VSCC). While the incidence of VSCC has remained relatively stable over the last three decades, the incidence of VIN has increased. VIN of usual type (uVIN) is human papillomavirus (HPV)-driven, affects younger women and is a multicentric disease. In contrast, VIN of differentiated type (dVIN) occurs in post-menopausal women and develops independent of HPV infection. dVIN often arises in a background of lichen sclerosus and chronic inflammatory dermatoses. Although isolated dVIN is significantly less common than uVIN, dVIN bears a greater risk for malignant transformation to VSCC and progresses over a shorter time interval. On histological examination, uVIN displays conspicuous architectural and cytological abnormalities, while the morphological features that characterise dVIN are much more subtle and raise a wide differential diagnosis. On the molecular level, dVIN is characterised by a higher number of somatic mutations, particularly in TP53. Here we review the classification, epidemiology, clinical features, histomorphology, ancillary markers and molecular genetics of both types of VIN, and discuss the morphological challenges faced by pathologists in interpreting these lesions.

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“…They are commonly associated with LSC and are considered precursors of verrucous carcinoma [7]. However, to date, both entities are still controversial due to their non-specific histological features which overlap with LSC, and their uncertain prognosis [8,9]. Initial reports suggested that the two etiopathogenic types of VSCC (HPVassociated and HPV-independent) could be separated using pure histological criteria.…”

Section: Introductionmentioning

confidence: 99%

HPV-independent Precursors Mimicking High-grade Squamous Intraepithelial Lesions (HSIL) of the Vulva

Rakislova

Alemany

Clavero

et al. 2020

American Journal of Surgical Pathology

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Two etiopathogenic types of vulvar squamous cell carcinoma (VSCC) have been described, human papillomavirus (HPV)-associated and HPV-independent. Precursor lesions, frequently identified in the adjacent skin, are also distinct in the two types of VSCC: high-grade squamous intraepithelial lesions (HSIL) in HPV-associated, and differentiated vulvar intraepithelial neoplasia (dVIN) or vulvar acanthosis with altered differentiation in HPV-independent VSCC. Although HPV-independent precursors mimicking HSIL have been described in the vulva, their frequency and morphological spectrum have not been completely characterized. We explored, in a large series of HPV-independent VSSC, the frequency and the histological features of precursors mimicking HSIL. We included 779 DNA HPV-negative/p16-negative VSCC with at least 1 cm of adjacent skin. We evaluated the histological and immunohistochemical (p16 and p53) characteristics of the intraepithelial lesions, focusing on precursors mimicking HPV-associated vulvar HSIL. 254 tumors (33%) had adjacent premalignant lesions. Of them, 186 (73%) had dVIN, 22 (9%) vulvar acanthosis with altered differentiation, and 46 (18%) lesions that mimicked HSIL. The mean age of the patients with these HSILlike lesions was 72 ± 15 years. Twenty-six of these HSIL-like lesions had basaloid morphology, 13 warty and 7 mixed basaloid/warty features. All the HSIL-like precursors were DNA HPV-negative/p16-negative, 74% of them showed p53 abnormal staining, and 35% of them had areas of conventional dVIN. In conclusion, about one-fifth of the HPV-independent precursors mimic HSIL, showing either basaloid or warty features.Older age, the presence of areas of typical HPV-independent intraepithelial lesions, together with p16 negativity should raise suspicion of HPV-independent etiology.

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Vulvar acanthosis with altered differentiation: is this entity a variant of hypertrophic lichen sclerosus?

Cited by 10 publications

References 4 publications

Vulval squamous cell carcinoma and its precursors

Vulval squamous cell carcinoma and its precursors

Squamous precursor lesions of the vulva: current classification and diagnostic challenges

HPV-independent Precursors Mimicking High-grade Squamous Intraepithelial Lesions (HSIL) of the Vulva

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