Immunophenotypic analysis of the p53 gene in non‐melanoma skin cancer and correlation with apoptosis and cell proliferation

Stratigos, A.; Kapranos, Nikiforos; Petrakou, Eftichia; Anastasiadou, A; Pagouni, A; Christofidou, Eleftheria; Petridis, Athanasios K.; Papadopoulos, Othon; Kokka, Eleni; Antoniou, Christina; Georgala, S.; Katsambas, A.

doi:10.1111/j.1468-3083.2005.01094.x

Cited by 34 publications

(42 citation statements)

References 29 publications

(60 reference statements)

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“…The Ki-67 antigen, a high molecular weight non-histone protein, is generally accepted to be a reliable marker of many types of proliferating cells [15] [16]. It is a nuclear structure expressed during all phases of the cell cycle (G 1 , S, G 2 and mitosis) but not by cells that are failing to undergo division.…”

Section: Discussionmentioning

confidence: 99%

Brm Inhibits the Proliferative Response of Keratinocytes and Corneal Epithelial Cells to Ultraviolet Radiation-Induced Damage

et al. 2014

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Ultraviolet radiation (UV) from sunlight is the primary cause of skin and ocular neoplasia. Brahma (BRM) is part of the SWI/SNF chromatin remodeling complex. It provides energy for rearrangement of chromatin structure. Previously we have found that human skin tumours have a hotspot mutation in BRM and that protein levels are substantially reduced. Brm−/− mice have enhanced susceptibility to photocarcinogenesis. In these experiments, Brm−/− mice, with both or a single Trp53 allele were exposed to UV for 2 or 25 weeks. In wild type mice the central cornea and stroma became atrophic with increasing time of exposure while the peripheral regions became hyperplastic, presumably as a reparative process. Brm−/−, Trp53+/−, and particularly the Brm−/− Trp53+/− mice had an exaggerated hyperplastic regeneration response in the corneal epithelium and stroma so that the central epithelial atrophy or stromal loss was reduced. UV induced hyperplasia of the epidermis and corneal epithelium, with an increase in the number of dividing cells as determined by Ki-67 expression. This response was considerably greater in both the Brm−/− Trp53+/+ and Brm−/− Trp53+/− mice indicating that Brm protects from UV-induced enhancement of cell division, even with loss of one Trp53 allele. Cell division was disorganized in Brm−/− mice. Rather than being restricted to the basement membrane region, dividing cells were also present in the suprabasal regions of both tissues. Brm appears to be a tumour suppressor gene that protects from skin and ocular photocarcinogenesis. These studies indicate that Brm protects from UV-induced hyperplastic growth in both cutaneous and corneal keratinocytes, which may contribute to the ability of Brm to protect from photocarcinogenesis.

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Section: Discussionmentioning

confidence: 99%

Brm Inhibits the Proliferative Response of Keratinocytes and Corneal Epithelial Cells to Ultraviolet Radiation-Induced Damage

et al. 2014

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“…The p53 protein detected through immunohistochemical staining represents stabilized and probably mostly mutant rather than wild-type p53 protein [38]. This is because wild-type protein has a very short half-life (5–20 min) and is not readily detectable by immunohistochemistry, while the mutated p53 gene encodes a protein with a substantially longer half-life (5–24 h) as indicated by p53 immunoreactivity [39,40,41]. Other authors [6] however have found no association between p53 expression in the epidermis and clinically assessed photoaging, which may be partly explained by a cruder system used in evaluating photoaging, and as acknowledged by the authors, by their exclusion of more severe clinical photoaging levels.…”

Section: Discussionmentioning

confidence: 99%

Comparison of Histological Measures of Skin Photoaging

Hughes¹,

Bredoux²,

Salas³

et al. 2011

Dermatology

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Background: Dermal elastosis is considered the histological ‘gold standard’ for evaluation of skin photoaging, but the relation of the level of dermal elastosis to other histological indicators of photoaging is not clear. Objective: To investigate how various proposed histological measures of photoaging compare with the level of dermal elastosis. Methods: Prospective, community-based study in Southeast Queensland, Australia, among 89 participants aged 40–82 years. Quantitative histology was used to evaluate 8 biomarkers of photoaged skin, and associations between grades of dermal elastosis and each of the other 7 biomarkers were analysed using ordinal logistic regression models with proportional odds assumption, using histological grades of elastosis as the outcome. Results: Older age, male sex and high outdoor exposure levels were confirmed as predictors ofhigh levels of dermal elastosis. After adjustment for age and sex, the only significant positive association with increasing elastosis grades was the proportion of p53-positive cells. Epidermal thickness, interdigitation index proportion of surface covered with melanin (% Fontana-Masson staining) and glycosaminoglycan content were not associated with elastosis in either crude or adjusted models. Conclusions: Amonga range of suggested biomarkers of photoaged skin, only p53-positive cells appear to be strongly associated with the level of dermal elastosis.

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“…The p53 tumor-suppressor gene is the classic example of these genes, as it is found mutated in 50-90% of human malignant tumors including skin cancers. [42327] The tumor-suppressor gene p53, located on the short arm of chromosome 17 (17p13.1), encodes for a nuclear protein which regulates cell proliferation by inhibiting cells entering S-phase. The p53 mutations are alleged to be the commonest genetic abnormality in human cancer.…”

Section: Discussionmentioning

confidence: 99%

Immunohistochemical evaluation of p53 and Ki67 expression in skin epithelial tumors

et al. 2013

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Background and Aims:The cellular mechanisms responsible for initiating or limiting the tumors including skin types are of great importance. The p53 is a tumor-inhibiting gene which is believed to be defective in many malignant situations. Ki67 is a non-histonic protein which is mainly interfere with the proliferation and has many controlling effects during the cell cycle. Because of their importance in skin tumor cell growth, this study aimed at evaluating the p53 and Ki67 expression in skin epithelial tumors by immunohistochemical method.Materials and Methods:In a descriptive setting, 50 biopsy samples (30 basal cell carcinomas (BCCs), 10 squamous cell carcinomas (SCCs), 8 keratoacanthomas (KAs), and 2 trichoepitheliomas (TEs)) were immunohistochemically evaluated for p53 and Ki67 expression during a 14-month period. The incidence and expression rate of these two variables were separately reported in each group of samples.Results:The expression rate of p53 was 67.77% for the BCCs, 50.20% for the SCCs, and null for the KAs. For both TEs, it was 50%. The expression rate of Ki67 was 57.33% for the BCCs, 47.70% for the SCCs, 37.5% for the KAs, and 0.0% for TEs. The incidence of P53+ cells was 100% and 90% in the BCC and SCC samples, respectively. The both TEs were positive in this regard. The incidence of Ki67+ cells was 100% for the BCC, SCC, and KA samples. The both TEs were negative in this regard.Conclusion:This study showed that the incidence rate of p53- and Ki67-positive cells is very high in skin malignant epithelial tumors. The expression rate of these two variables is comparable with reports in the literature. Further studies with large sample size are recommended to be carried out for KA and TE samples.

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Immunophenotypic analysis of the p53 gene in non‐melanoma skin cancer and correlation with apoptosis and cell proliferation

Cited by 34 publications

References 29 publications

Brm Inhibits the Proliferative Response of Keratinocytes and Corneal Epithelial Cells to Ultraviolet Radiation-Induced Damage

Brm Inhibits the Proliferative Response of Keratinocytes and Corneal Epithelial Cells to Ultraviolet Radiation-Induced Damage

Comparison of Histological Measures of Skin Photoaging

Immunohistochemical evaluation of p53 and Ki67 expression in skin epithelial tumors

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