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p53 expression in odontogenic keratocyst epithelium
T J Li1, R M Browne, S S Prime
1Unit of Oral Pathology, School of Dentistry, University of Birmingham, Queensway, England.
Summary
p53 protein is overexpressed in odontogenic keratocysts (OKC) compared to radicular and dentigerous cysts, but without detectable p53 gene mutations. This suggests p53 protein stabilization or overproduction in OKC epithelium.
Area of Science:
- Oral Pathology
- Molecular Biology
- Oncology
Background:
- Odontogenic keratocysts (OKC) exhibit aggressive behavior.
- The role of p53 protein in OKC development is not fully understood.
- p53 protein expression can indicate cellular abnormalities.
Purpose of the Study:
- To investigate p53 protein expression in OKC, radicular cysts (RC), and dentigerous cysts (DC).
- To determine if p53 gene mutations correlate with p53 protein overexpression in OKC.
- To analyze the distribution and significance of p53 protein in different cyst types.
Main Methods:
- Immunohistochemistry using three distinct p53 antibodies (BP53-12, 1801, CM1) on paraffin-embedded cyst sections.
- Quantitative analysis of p53-positive cells using TV image analysis.
- Polymerase chain reaction-single-strand conformation polymorphism (PCR-SSCP) and direct sequencing to detect p53 gene mutations in exons 5-10.
Main Results:
- Clone BP53-12 demonstrated consistent nuclear p53 staining in all cyst types, with significantly higher expression in OKC compared to RC and DC.
- p53-positive cells in OKC were predominantly suprabasal, differing from RC and DC.
- No p53 gene mutations were detected in exons 5-10 of OKC, RC, or normal oral mucosa samples.
- A significant correlation was observed between p53 and Ki67 labeling in OKC when NBCCS-related cysts were excluded.
Conclusions:
- Overexpression of p53 protein in OKC epithelium, detected via immunocytochemistry, is not linked to p53 gene mutations.
- The observed p53 protein overexpression likely results from stabilization or overproduction of the normal p53 protein.
- These findings contribute to understanding the molecular mechanisms underlying OKC pathogenesis.