Expression of p53 and Proliferating Cell Nuclear Antigen in Lichen Sclerosus et Atrophicus With Different Histological Features

Soini, Ylermi; Pääkkö, Paavo; Vähäkangas, Kirsi; Vuopala, Salme; Lehto, Veli‐Pekka

doi:10.1097/00004347-199407000-00002

Cited by 20 publications

(11 citation statements)

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“…Soini et al. 17 looking at p53 expression in LS, showed no p53 expression in normal vulval skin used as a control. Similarly, when using proliferating cell nuclear antigen as a proliferation marker, all normal vulval samples demonstrated some proliferation in the basal/parabasal keratinocytes; however, only < 15% of the overall cell population showed proliferation.…”

Section: Discussionmentioning

confidence: 99%

The effect of topical corticosteroids on Ki67 and p53 expression in vulval lichen sclerosus

Rolfe¹,

Crow

Reid³

et al. 2002

Br J Dermatol

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Section: Discussionmentioning

confidence: 99%

The effect of topical corticosteroids on Ki67 and p53 expression in vulval lichen sclerosus

Rolfe¹,

Crow

Reid³

et al. 2002

Br J Dermatol

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“…[19] Vulvar skin affected by LS has a wide range of proliferative capacity. [20] The p53 and proliferating cell nuclear antigens are altered in VLS, resulting in changes of the epidermal cell proliferative capacity. Antibody formation against extracellular matrix protein 1 may contribute to disease progression[21] seen in roughly 75% of women with VLS.…”

Section: Etiologymentioning

confidence: 99%

Vulvar lichen sclerosus et atrophicus

Nair

2017

J Mid-life Health

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Vulvar lichen sclerosus (VLS) is a chronic inflammatory dermatosis characterized by ivory-white plaques or patches with glistening surface commonly affecting the vulva and anus. Common symptoms are irritation, soreness, dyspareunia, dysuria, and urinary or fecal incontinence. Anogenital lichen sclerosus (LS) is characterized by porcelain-white atrophic plaques, which may become confluent extending around the vulval and perianal skin in a figure of eight configuration. Thinning and shrinkage of the genital area make coitus, urination, and defecation painful. LS is not uncommon in India and present as an itchy vulvar dermatosis which a gynecologist may mistake for candidal vulvovaginitis. There is often a delay in diagnosis of VLS due to its asymptomatic nature and lack of awareness in patients as well as physicians. Embarrassment of patients due to private nature of the disease and failure to examine the genital skin properly are the other reasons for delay in diagnosis. There is no curative treatment for LS. Various medications available only relieve the symptoms. Chronic nature of the disease affects the quality of life. Proper and regular follow-up is required as there are chances of the development of squamous cell carcinoma.

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“…A study of epidermal differentiation using keratin markers showed that keratins 6 and 16, associated with increased cell turnover, were expressed suprabasally, and keratins 1 and 10, markers of cornifying epithelium, persisted in spite of the apparent atrophy of the epidermis. Soini et al (1994) have shown, in a study of proliferating cell nuclear antigen, that vulval skin affected by lichen sclerosus has a wide range of proliferative capacity and that high levels are associated with overexpression of wild-type p53. Tan et al (1994) also showed an altered p53 expression and epidermal cell proliferation in vulval lichen sclerosus, compared with normal vulval skin and with extragenital lichen sclerosus.…”

Section: Aetiologymentioning

confidence: 99%