PubMed · 2007 · 31 citations · 24 references
MedicineOncologyOral PathologyCarcinogenesisMolecular OncologyOral OncologyOral Cancer PathologyOral Cancer PrognosisOral CarcinogenesisOral Cavity CancerOral NeoplasiaSquamous Cell CarcinomaMucosal DysplasiaOral Epithelial CarcinogenesisOral Lesion Malignant TransformationP16 ExpressionPremalignant Oral LesionsPrognostic Marker AssessmentPrognostic Marker Evaluation
BACKGROUND: The p16 tumour suppressor gene is known to be involved in regulation of the cell cycle. p16 expression in sequential histological stages of oral squamous cell carcinoma (OSCC) formation was investigated using an experimental model of induced oral carcinogenesis in Syrian golden hamsters. MATERIALS AND METHODS: Thirty-seven animals were divided into one control group (N = 7) and three experimental groups (N = 10 each) which were treated with a carcinogen and sacrificed at 10, 14 and 19 weeks after treatment. Tumour sections were studied immunohistochemically using monoclonal antibodies against p16 protein. RESULTS: p16 was found significantly increased in hyperplasia, sharply decreased in dysplasia and in the subsequent stages of oral carcinogenesis. CONCLUSION: Inactivation of p16 occurs at the early stage of oral mucosal dysplasia in the multistep process of oral tumourigenesis. Therefore, p16 may be considered as a useful prognostic marker for the progression of oral cancer.
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Ahmedin Jemal, Freddie Bray, Jacques Ferlay et al. · CA A Cancer Journal for Clinicians · 2011 · 55K citations · Full text
Oncogenic ras Provokes Premature Cell Senescence Associated with Accumulation of p53 and p16INK4a
Manuel Serrano, Athena W. Lin, Mila E. McCurrach et al. · Cell · 1997 · 5.1K citations · Full text
Medicine, Cell Biology, Oncology +10
Oral Cavity and Esophageal Carcinogenesis Modeled in Carcinogen-Treated Mice
Xiao‐Han Tang, Beatrice S. Knudsen, Debra L. Bemis et al. · Clinical Cancer Research · 2004 · 394 citations
Medicine, Cancer Biology, Oncology +13