Abstract | BACKGROUND: The expression of tumour suppressor p53 and oncogene c-myc was investigated in an experimental model of chemically induced carcinogenesis in normal and diabetic (type I) Sprague-Dawley rats. MATERIALS AND METHODS: RESULTS: From hyperplasia to later stages of oral oncogenesis, mutant p53 expression was at higher levels in diabetic rats in comparison to normal animals, although the pattern of expression was similar. In contrast, c-myc expression was significantly higher in diabetic than in normal rats only in normal mucosa and hyperplasia. CONCLUSION: It seems that diabetes contributed to increased accumulation of mutations in the p53 gene, contributing to increased proliferation of tumour cells during oral oncogenesis. Additionally, diabetes appeared to enhance c-myc expression only in the initial stages of oral oncogenesis.
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Authors | Eleftherios Vairaktaris, Giorgos Kalokerinos, Lambros Goutzanis, Sofia Spyridonidou, Stavros Vassiliou, Spyridoula Derka, Emeka Nkenke, Christos Yapijakis, Antonis Vylliotis, Andreas Lazaris, Efstratios Patsouris |
Journal | Anticancer research
(Anticancer Res)
2007 May-Jun
Vol. 27
Issue 3B
Pg. 1465-73
ISSN: 0250-7005 [Print] Greece |
PMID | 17595763
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- MYC protein, human
- Proto-Oncogene Proteins c-myc
- Tumor Suppressor Protein p53
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Topics |
- Animals
- Carcinoma, Squamous Cell
(chemistry, metabolism, pathology)
- Cell Transformation, Neoplastic
(chemistry, metabolism, pathology)
- Diabetes Mellitus, Type 1
(metabolism)
- Disease Models, Animal
- Female
- Immunohistochemistry
- Mouth Mucosa
(chemistry, metabolism, pathology)
- Mouth Neoplasms
(chemistry, metabolism, pathology)
- Proto-Oncogene Proteins c-myc
(analysis, metabolism)
- Rats
- Rats, Sprague-Dawley
- Tumor Suppressor Protein p53
(analysis, metabolism)
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