High levels of p53 expression correlate with DNA aneuploidy in (pre)malignancies of the vulva

Avoort, Irene A.M. van der; Nieuwenhof, H.P. van de; Otte-Höller, Irene; Nirmala, Ella; Bulten, Johan; Massuger, Leon F.A.G.; Laak, Jeroen van der; Slootweg, Piet J.; Hullu, Joanne A. de; Kempen, Léon C van

doi:10.1016/j.humpath.2009.12.015

Cited by 20 publications

(10 citation statements)

References 28 publications

(38 reference statements)

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“…This is contrast to lichen sclerosus, of which the percentage of p53-positive cells did not exceed 30%. 16 In conclusion, we found that in patients with progression, the original diagnosis of lichen sclerosus was often revised into differentiated VIN. When adhering to strict criteria (elongated rete ridges with anastomosis, a disorderly basal cell layer, dyskeratosis and parakeratosis, prominent nucleoli and atypical mitosis), the diagnosis of differentiated VIN should be more easy to make, especially when the patient is suffering from lichen sclerosus as well.…”

Section: Discussionmentioning

confidence: 79%

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: 79%

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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“…Epidemiological data confirm two different pathways for vulvar SCC analogous to the two types of VIN: one related to HPV infection and one independent [6,9,10,13,14,15,16]. HPV-related SCC has a mean age of 63.3 years and it is usually warty-basaloid in type, while HPV-independent SCC has a mean age of 70.2 years and it is usually of the keratinizing type.…”

Section: Vulvar Oncogenesismentioning

confidence: 99%

Vulvar intraepithelial neoplasia

Preti

Scurry²,

Marchitelli

et al. 2014

Best Practice & Research Clinical Obstetrics & Gynaecol

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“…42 In short, after fixation of cells in Böhm fixative and staining with Schiff reagent, DNA image cytometry was performed with Q-path DNA software to determine DNA ploidy of the nuclei (Leica Imaging Systems Ltd, Cambridge, UK).…”

Section: Dna Image Cytometrymentioning

confidence: 99%

Lithium Causes G2 Arrest of Renal Principal Cells

Groot

Alsady

Jaklofsky

et al. 2014

Journal of the American Society of Nephrology

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Vasopressin-regulated expression and insertion of aquaporin-2 channels in the luminal membrane of renal principal cells is essential for urine concentration. Lithium affects urine concentrating ability, and approximately 20% of patients treated with lithium develop nephrogenic diabetes insipidus (NDI), a disorder characterized by polyuria and polydipsia. Lithium-induced NDI is caused by aquaporin-2 downregulation and a reduced ratio of principal/intercalated cells, yet lithium induces principal cell proliferation. Here, we studied how lithium-induced principal cell proliferation can lead to a reduced ratio of principal/intercalated cells using two-dimensional and three-dimensional polarized cultures of mouse renal collecting duct cells and mice treated with clinically relevant lithium concentrations. DNA image cytometry and immunoblotting revealed that lithium initiated proliferation of mouse renal collecting duct cells but also increased the G2/S ratio, indicating G2/M phase arrest. In mice, treatment with lithium for 4, 7, 10, or 13 days led to features of NDI and an increase in the number of principal cells expressing PCNA in the papilla. Remarkably, 30%-40% of the PCNA-positive principal cells also expressed pHistone-H3, a late G2/M phase marker detected in approximately 20% of cells during undisturbed proliferation. Our data reveal that lithium treatment initiates proliferation of renal principal cells but that a significant percentage of these cells are arrested in the late G2 phase, which explains the reduced principal/intercalated cell ratio and may identify the molecular pathway underlying the development of lithium-induced renal fibrosis.

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High levels of p53 expression correlate with DNA aneuploidy in (pre)malignancies of the vulva

Cited by 20 publications

References 28 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

Vulvar intraepithelial neoplasia

Lithium Causes G2 Arrest of Renal Principal Cells

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