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1 Department of Oral & Maxillofacial Surgery, Massachusetts General Hospital/Harvard School of Dental Medicine, 188 Longwood Avenue, Boston, MA 02115; 2 Department of Pathology, Harvard Medical School, 200 Longwood Avenue, Boston, MA 02115; 3 Gastroenterology Division, 4 Department of Genetics, and 5 Cancer Center, University of Pennsylvania, 415 Curie Blvd., Philadelphia, PA 19104; 6 Department of Oral Diagnostic Sciences, Division of Oral Pathology, Harvard School of Dental Medicine, 188 Longwood Avenue, Boston, MA 02115;
* corresponding author, randy_todd{at}hms.harvard.edu
The dysregulation of the molecular events governing cell cycle control is emerging as a central theme of oral carcinogenesis. Regulatory pathways responding to extracellular signaling or intracellular stress and DNA damage converge on the cell cycle apparatus. Abrogation of mitogenic and anti-mitogenic response regulatory proteins, such as the retinoblastoma tumor suppressor protein (pRB), cyclin D1, cyclin-dependent kinase (CDK) 6, and CDK inhibitors (p21WAF1/CIP1, p27KIP1, and p16INK4a), occur frequently in human oral cancers. Cellular responses to metabolic stress or genomic damage through p53 and related pathways that block cell cycle progression are also altered during oral carcinogenesis. In addition, new pathways and cell cycle regulatory proteins, such as p12DOC-1, are being discovered. The multistep process of oral carcinogenesis likely involves functional alteration of cell cycle regulatory members combined with escape from cellular senescence and apoptotic signaling pathways. Detailing the molecular alterations and understanding the functional consequences of the dysregulation of the cell cycle apparatus in the malignant oral keratinocyte will uncover novel diagnostic and therapeutic approaches.
Key words. Oral cancer, cell cycle, proliferation, apoptosis, senescence
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