Abstract
In normal oral epithelium the cells divide, mature, differentiate, and die. This sequence is not normally followed in oral cancer. Instead, the death of the cells is somehow prevented, although the pathways toward cell death in normal oral epithelium and the defects in oral cancer are not well defined. However, several components in the system have been identified, and information on their interactions is becoming available. This review summarizes the evidence for cell death being due to apoptosis and the central role of the p53 gene product in its regulation. Areas for future research are also identified.
MeSH terms
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Apoptosis / genetics
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Apoptosis / physiology*
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Carcinoma, Squamous Cell / genetics
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Carcinoma, Squamous Cell / metabolism*
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Carcinoma, Squamous Cell / pathology
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Cell Survival
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Cell Transformation, Neoplastic
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Cyclin D1 / metabolism
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Cyclin-Dependent Kinase Inhibitor p21
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Cyclins / metabolism
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ErbB Receptors / metabolism
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Gene Expression Regulation, Neoplastic*
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Humans
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Mouth Neoplasms / genetics
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Mouth Neoplasms / metabolism*
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Mouth Neoplasms / pathology
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Neoplasm Proteins / genetics
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Neoplasm Proteins / metabolism*
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Nuclear Proteins*
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Papillomaviridae / physiology
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Proto-Oncogene Proteins / metabolism
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Proto-Oncogene Proteins c-bcl-2*
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Proto-Oncogene Proteins c-mdm2
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Proto-Oncogene Proteins c-myc / metabolism
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Tumor Suppressor Protein p53 / genetics
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Tumor Suppressor Protein p53 / metabolism*
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bcl-2-Associated X Protein
Substances
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CDKN1A protein, human
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Cyclin-Dependent Kinase Inhibitor p21
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Cyclins
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Neoplasm Proteins
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Nuclear Proteins
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Proto-Oncogene Proteins
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Proto-Oncogene Proteins c-bcl-2
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Proto-Oncogene Proteins c-myc
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Tumor Suppressor Protein p53
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bcl-2-Associated X Protein
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Cyclin D1
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MDM2 protein, human
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Proto-Oncogene Proteins c-mdm2
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ErbB Receptors