Scientific Articles
Prevalence 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*,**

https://doi.org/10.1053/joms.2002.31851Get rights and content

Abstract

Purpose: Loss of normal p53 is correlated to the progression of several preneoplastic lesions to neoplasms, and overexpression of bcl-2 determines an alteration of programmed cell death. There is an increased awareness of the importance of apoptosis in cancerogenesis, and a strong correlation of Ki-67 with high tumor grade has been reported. Materials and Methods: The aim of our study was to investigate immunohistochemically the expression and relationship of p53, bcl-2, MIB-1, and the apoptotic index (AI) in normal oral epithelium, leukoplakia, dysplasia, and oral squamous cell carcinoma. Results: A strong correlation was found between p53 overexpression and cell proliferation (MIB-1) and the AI. An inverse relationship was found between bcl-2 expression and MIB-1 and AI. A significant inverse relationship was found between p53 and bcl-2. A good positive correlation was present between AI and MIB-1 expression. Conclusions: Apoptosis could be important to help to understand oral carcinogenesis. © 2002 American Association of Oral and Maxillofacial Surgeons J Oral Maxillofac Surg 60:532-540, 2002

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).

. Normal oral mucosa, showing a few basal cells positive to p53 (arrows) (p53 immunostaining alkaline phosphatase antialkaline

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

References (26)

  • ATC Chan et al.

    Assessment of proliferating nuclear antigen in nasopharyngeal carcinoma tissue and its relation to clinical findings

    Oral Oncol

    (1997)
  • HJ Harn et al.

    Apoptosis occurs more frequently in intraductal carcinoma than in infiltrating duct carcinoma of human breast cancer and correlates with altered p53 expression detected by terminal-deoxynucleotidyl-transferase-mediated dUTP-FITC nick end labeling (TUNEL)

    Histopathology

    (1997)
  • W Tjalma et al.

    Prognostic value of bcl-2 expression in patients with operable carcinoma of the uterine cervix

    J Clin Pathol

    (1997)
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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.

    **

    Address correspondence and reprint requests to Dr Piattelli: Via F. Sciucchi 63, 66100 Chieti, Italy; e-mail: [email protected]

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