Scientific ArticlesPrevalence of p53, bcl-2, and Ki-67 immunoreactivity and of apoptosis in normal oral epithelium and in premalignant and malignant lesions of the oral cavity*,**
Section snippets
Materials and methods
A total of 70 biopsy samples were analyzed. The following formalin-fixed, paraffin-embedded tissues were used in this study: normal oral mucosa obtained during third molar removal (10 cases), leukoplakia (12 cases), epithelial dysplasia (12 cases: 6 mild and 6 severe dysplasia and carcinoma in situ), invasive carcinoma well differentiated (G1) (12 cases), invasive carcinoma moderately differentiated (G2) (12 cases), and invasive carcinoma poorly differentiated (G3) (12 cases). The age of the
p53
p53 was present in the basal layer in normal oral epithelium; in the basal and parabasal layers in leukoplakia, dysplasia, and carcinoma in situ; and in central and peripheral regions in invasive carcinoma. In normal oral epithelium in only 1 sample, the positivity was between 5% and 50%, whereas all of the other specimens showed a positivity of less than 5% (Fig 1).
Discussion
Ramsay et al3 showed that compared with nevi, in which the bcl-2 protein immunoreactivity was present in all cells, melanomas exhibited a progressive loss of the protein expression with increased levels of malignancy. These data suggest, perhaps, that bcl-2 loss is associated with or reflects an increased malignant potential3. The presence of bcl-2 seems to be associated with a better prognosis in some tumors but not in others.2, 3, 16 High levels of bcl-2 protein correlated with lower rates of
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2014, Pathology Research and PracticeCitation Excerpt :It is not however a marker of transition to carcinoma. Highest Ki67 is seen in severe dysplasia and shows an inverse relationship with Bcl-2 an inverse relationship with Bcl-2 and P53 has also been noted in many tissue including breast, colon, stomach, esophagus, thyroid and lymphoma [17]. Ki67 and ProexC have been used together as a diagnostic adjunct in esophageal squamous intraepithelial neoplasia [7].
Oral leukoplakia in a patient with Fanconi anemia: Recurrence or a new primary lesion?
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Immunohistochemical study of syndecan-1 down-regulation and the expression of P35 protein in oral lichen planus: a clinicopathologic correlation with hepatitis C infection in the Egyptian population
2010, Annals of Diagnostic PathologyCitation Excerpt :These mutations may result in the formation of defective, highly stabilized protein with an increased half-life time in tissues compared with the 20 minutes for the wild-type protein. This is the basis for the use of immunohistochemistry that can detect mutant p53 products [25], which are indicative of mutant protein [26]. Other mechanisms may similarly stabilize the protein and so increase the amount detected, whereas conversely, deletion of p53 gene (“null allele”) may produce a false-negative result [27].
ERBB receptors in developing, dysplastic and malignant oral epithelia
2008, Oral OncologyCitation Excerpt :The Mib-1 index did not correlate with corresponding EGFR and ERBB2-4 receptor staining, or with the histopathological diagnosis relating to the sample. However, the Mib-1 index followed previously reported curves of mean values for dysplasias and OSCCs.37 The DNA contents of DOK cells were studied to allow evaluation of the severity of genetic changes in the cell line.
Computer-assisted analysis of cell proliferation markers in oral lesions
2007, Acta Histochemica
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This work was supported in part by the National Research Council (CNR), Rome, Italy, and by the Ministry of University, Research, Science and Technology (MURST), Rome, Italy.
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Address correspondence and reprint requests to Dr Piattelli: Via F. Sciucchi 63, 66100 Chieti, Italy; e-mail: [email protected]