Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P04637 (p53)
 77,613 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Oral lichen planus (OLP) is a chronic inflammatory disease, which has been clinically associated with development to oral cancer. A double immunofluorescence labeling study found that 8-nitroguanine and 8-oxo-7,8-dihydro-2'-deoxyguanosine (8-oxodG) accumulated in oral epithelium in OLP and oral squamous cell carcinoma (OSCC) biopsy specimens, whereas little or no immunoreactivity was observed in normal oral mucosa. Colocalization of 8-nitroguanine and inducible nitric oxide synthase (iNOS) was found in oral epithelium of OLP and OSCC. Immunoreactivity of 3-nitrotyrosine, which is formed by protein tyrosine nitration and is considered to be a biochemical marker for inflammation, was also observed in oral epithelial cells and colocalized with 8-nitroguanine. Accumulation of p53 was more strongly observed in oral epithelium in OSCC than OLP, whereas there was no p53 accumulation in normal oral mucosa. Our findings demonstrate that iNOS-dependent DNA damage in OLP may lead to p53 accumulation in not only OLP but also OSCC. We conclude that the formation of potentially mutagenic DNA lesions including 8-nitroguanine and 8-oxodG may contribute to the development of oral cancer from OLP.
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PMID:Nitrative and oxidative DNA damage in oral lichen planus in relation to human oral carcinogenesis. 1612 40

The study aimed to assess the proliferative activity and karyotype in Oral Lichen Planus (OLP) lesions. G-banding chromosomal analysis of short-term primary cultures, and immunohistochemical expression of Ki67 and p53 were applied in 30 consecutive OLP patients divided into two groups according to clinical presentation of the lesions, and in nine subjects as negative controls. Mean values of Ki67 and p53 expression differed significantly (P<.01) between controls and patients groups with reticular or atrophic-erosive forms of OLP, whereas there was no significant difference between the two groups of patients with reticular or atrophic-erosive lesions. Six OLP patients showed clonal chromosome alterations, four of them associated with p53 overexpression. In conclusion, OLP is characterized by a high cellular turnover in most patients irrespective of clinical disease presentation. The genetic instability found in some patients should be interpreted as a consequence of the enhanced epithelial turnover, although we cannot rule out the possibility that some of the cytogenetic non-random anomalies observed represent early steps in cancer development.
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PMID:High proliferative activity and chromosomal instability in oral lichen planus. 1709 90

Oral lichen planus (OLP) is a chronic inflammatory disease of unknown origin, showing little spontaneous regression. WHO classifies OLP as a premalignant condition, however, the underlying mechanisms initiating development of cancer in OLP lesions are not understood. The p53 tumour suppressor plays an important role in many tumours, and an increased expression of p53 protein has been seen in OLP lesions. Recently it was shown that the human TP53 gene encodes at least nine different isoforms. Another member of the p53 family, p63, comprises six different isoforms and plays a crucial role in the formation of oral mucosa, salivary glands, teeth and skin. It has also been suggested that p63 is involved in development of squamous cell carcinoma of the head and neck (SCCHN). In contrast to p53, a decreased expression of p63 protein has been seen in OLP lesions. In this study, we mapped the expression of five novel p53 isoforms at RNA and protein levels in OLP and matched normal controls. In the same samples we also measured levels of p63 isoforms using quantitative RT-PCR. Results showed p53 to be expressed in all OLP lesions and normal tissues. The p53 beta and delta 133p53 isoforms were expressed in the majority of samples whereas the remaining three novel isoforms analysed were expressed in only a few samples. Levels of p63 isoforms were lower in OLP lesions compared with normal tissue, however, changes were not statistically significant.
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PMID:Expression of novel p53 isoforms in oral lichen planus. 1741 19

Oral lichen planus (OLP) is a relatively common chronic disease of the oral mucosa for which the aetiopathogenesis is not fully understood. It mainly affects middle aged and elderly. The finding of autoantibodies against p63, a member of the p53 family, is a strong indication of autoimmunity as a causative or contributing factor. The WHO classified OLP as a potentially malignant disorder, but still there is an ongoing debate in the literature on this subject. The TP53 gene encodes a tumour suppressor protein that is involved in induction of cell-cycle arrest or apoptosis of DNA-damaged cells. The p63 gene encodes six different proteins that are crucial for formation of the oral mucosa and skin. The coordinated stabilization of p53 and decreased expression of p63 seen in OLP cause induction of apoptosis enabling removal of DNA-damaged cells. In view of the complexity of cancerogenesis, no firm statement can at present be made about the relevance of the observed relationship between p53 and p63 and the possible malignant transformation of OLP.
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PMID:Oral lichen planus and the p53 family: what do we know? 2172 87

Oral lichen planus (OLP) is considered as a premalignant lesion, but some argue that only lichenoid lesions with dysplasia is precancerous. To address the question whether OLP without dysplasia is premalignant, we investigated the immunohistochemical expression of p53 in OLPs without dysplasia. Half of the OLPs showed p53 positive cells in the basal epithelium. SSCP-PCR analysis of 4 p53 positive OLPs failed to demonstrate mutations. What is the significance of p53 expression in these OLPs? The confinement of p53 positive cells to the basal cells seems to be against false positivity. Since the pathogenesis of OLPs involves cell-mediated cytotoxicity (CMC) which causes marked apoptosis, it is possible that the p53 expression represents wild-type p53 that may be regulating the apoptosis. Alternatively p53 protein may be stabilized by some mechanisms other than gene mutation as a result of cellular insults from CMC.
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PMID:p53 overexpression in oral lichen planus. 2159 27

Oral lichen planus (OLP) represents a common mucocutaneous disease. Various authors have suggested that OLP has malignant potential; however, the mechanisms involved in malignant transformation have not yet been elucidated. A 79-year-old man presented a white lesion for five months in the buccal mucosa diagnosed as OLP. After two months using 0.05% clobetasol ointment for treatment, the lesion became ulcerated. A new biopsy of the same lesion was performed, and histological analysis showed an in situ oral carcinoma (ISOC). An immunohistochemistry panel was performed, and p16 expression was negative in OLP, however, it showed weak cytoplasmic staining in ISOC. There was strong nuclear BUB3 staining in both OLP and ISOC areas. p53 showed less intense nuclear staining in both regions. Ki67 was negative in OLP area, but showed nuclear staining in the ISOC. SOX4 was negative in both studied areas. BUB3 expression, first reported in this case, and the p16 expression may suggest some influence of these genes on pathogenesis or malignant potential of OLP.
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PMID:In situ carcinoma developed over oral lichen planus: a case report with analysis of BUB3, p16, p53, Ki67 and SOX4 expression. 2639 19

Oral lichen planus (OLP) and oral lichenoid reaction (OLR) are clinically and histopathologically similar diseases. Whereas OLP is a consequence of T cell mediated autoinflammatory process to a still unknown antigen, OLR might be caused by drugs, dental restorative materials and dental plaque. Pubmed was searched and 24 publications published over the last three years regarding etiology, diagnosis and malignant alteration were included in this study. Patients with OLR who have amalgam fillings near lesions should have them replaced, i.e. when possible they should be referred to patch test, as well as when drug-induced OLR are suspected. OLR lesions induced by drugs should disappear when the offending drug has been discontinued. Histology finding in OLR consists of more eosinophils, plasma cells and granulocytes in comparison to OLP lesions. Furthermore, OLP lesions showed more p53, bcl-2 and COX-2 positivity when compared to OLR. OLP is characterized by infiltration, atrophic epithelium, rete pegs and Max Joseph spaces, while deep infiltration into connective tissue and hyperkeratosis were the criteria for making the diagnosis of OLR. The number of degranulated mastocytes in the reticular layer, as well as the number of capillaries was higher in OLR in comparison to OLP. It seems that OLR are more prone to malignant alteration in comparison to OLP.
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PMID:ORAL LICHEN PLANUS AND ORAL LICHENOID REACTION--AN UPDATE. 2701 28