Abstract:Leukoplakias are oral lesions that may have many clinical and histological aspects and they are usually associated with malignancy when dysplastic alterations are shown. However, these transformations may occur in non-dysplastic lesions that show harmless clinical aspect. For this reason, the proposal was to study the p53 and PCNA immunohistochemical expression in non-dysplastic leukoplakias, trying to correlate the results only with the epithelial keratinization degree. For this, 24 leukoplakias degrees I, II… Show more
“…However, overexpression of p53 mutant protein has been demonstrated in precancerous and cancerous lesions of the oral cavity (Lawall Mde and Crivelini, 2006). Our results were in line with these observations.…”
<p>The present study evaluated the anti-proliferative and apoptotic effect of quinine on oral cancer cells Hep-2 and KB. Cell inhibition, apoptosis and anti-inflammatory effects were explored by nuclear DNA cleavage, condensation, change in membrane potential of mitochondria. Meanwhile, inflammatory and apoptosis-related mRNA and proteins expressions such as iNOS COX-2, IL-6, Bcl-2, mutant p53, Bax, caspase-3 and NF-κB were determined by RT-PCR and Western blotting assays. Results showed that, quinine treatment significantly inhibited the cell viability and colony formation, inhibited cell proliferation lead to increased generation of reactive oxygen species induction of MMP depolarization, morphological changes and DNA damage in dose- and time-dependent manner. Moreover, quinine significantly decreased the iNOS, COX-2, IL-6, Bcl-2 and mutant p53 simultaneously up-regulated Bax, caspase-3 expressions through the inhibition of NF-κB suggest that quinine may serve as a potential candidate in the prevention of cell proliferation and enhances apoptosis via inhibiting up-stream signalling.</p><p><strong>Video Clip</strong></p><p><a href="https://youtube.com/v/83HX2fFTXkg">Programmed cell death assay by dual staining:</a> 17 min 25 sec</p><p> </p>
“…However, overexpression of p53 mutant protein has been demonstrated in precancerous and cancerous lesions of the oral cavity (Lawall Mde and Crivelini, 2006). Our results were in line with these observations.…”
<p>The present study evaluated the anti-proliferative and apoptotic effect of quinine on oral cancer cells Hep-2 and KB. Cell inhibition, apoptosis and anti-inflammatory effects were explored by nuclear DNA cleavage, condensation, change in membrane potential of mitochondria. Meanwhile, inflammatory and apoptosis-related mRNA and proteins expressions such as iNOS COX-2, IL-6, Bcl-2, mutant p53, Bax, caspase-3 and NF-κB were determined by RT-PCR and Western blotting assays. Results showed that, quinine treatment significantly inhibited the cell viability and colony formation, inhibited cell proliferation lead to increased generation of reactive oxygen species induction of MMP depolarization, morphological changes and DNA damage in dose- and time-dependent manner. Moreover, quinine significantly decreased the iNOS, COX-2, IL-6, Bcl-2 and mutant p53 simultaneously up-regulated Bax, caspase-3 expressions through the inhibition of NF-κB suggest that quinine may serve as a potential candidate in the prevention of cell proliferation and enhances apoptosis via inhibiting up-stream signalling.</p><p><strong>Video Clip</strong></p><p><a href="https://youtube.com/v/83HX2fFTXkg">Programmed cell death assay by dual staining:</a> 17 min 25 sec</p><p> </p>
“…During the immunohistochemical analysis of the AC cases, we observed that p53 protein expression occurred in both basal and suprabasal layer epithelial cells. Equal immunolocalization has been obtained by other authors in different cases of premalignant oral lesions 6 , 9 , 14 , 15 , 23 , although Argawal, et al 2 (1998) observed that the p53 protein was only expressed in the nucleus of basal layer epithelial cells in cases of oral leukoplasias. It is implied that p53 protein expression in keratinocytes, and not in differentiated cells, supports the potential role of p53 in preventing early carcinogenesis 31 .…”
Actinic cheilitis is a potentially malignant lip lesion caused by excessive and prolonged exposure to ultraviolet radiation, which can lead to histomorphological alterations indicative of abnormal cell differentiation. In this pathology, varying degrees of epithelial dysplasia may be found. There are few published studies regarding the p53 and MDM2 proteins in actinic cheilitis. Fifty-eight cases diagnosed with actinic cheilitis were histologically evaluated using Banóczy and Csiba (1976) parameters, and were subjected to immunohistochemical analysis using the streptavidin-biotin method in order to assess p53 and MDM2 protein expression. All studied cases expressed p53 proteins in basal and suprabasal layers. In the basal layer, the nuclei testing positive for p53 were stained intensely, while in the suprabasal layer, cells with slightly stained nuclei were predominant. All cases also tested positive for the MDM2 protein, but with varying degrees of nuclear expression and a predominance of slightly stained cells. A statistically significant correlation between the percentage of p53 and MDM2-positive cells was established, regardless of the degree of epithelial dysplasia. The expression of p53 and MDM2 proteins in actinic cheilitis can be an important indicator in lip carcinogenesis, regardless of the degree of epithelial dysplasia.
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