The molecular biology of oral carcinogenesis: toward a tumor progression model.
An understanding of the molecular basis of oral carcinogenesis will alter our clinical approach to oral cancer. The nomenclature and major themes of molecular oral tumor biology are reviewed, beginning with the regulation events governing normal cellular physiology. In carcinogenesis, chromosomal or cytogenetic alterations lead to deregulation of tightly controlled stimulatory and inhibitory pathways, growth-promoting proto-oncogenes are mutated into overactive oncogenes, and growth-suppressing or tumor suppressor genes are inactivated. Recent advances in defining these fundamental mechanisms of tumor biology may allow prevention, diagnosis, and treatment of oral cancer to be approached at the molecular level.
Todd
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Department of Oral and Maxillofacial Surgery, Massachusetts General Hospital, Boston, USA.
Donoff
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RB
Wong
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DT
D016588:Anticarcinogenic Agents / Q000627:therapeutic use; D002294:Carcinoma, Squamous Cell / Q000235:genetics*; D004273:DNA, Neoplasm / Q000235:genetics; D018450:Disease Progression; D066246:ErbB Receptors / Q000096:biosynthesis; D015972:Gene Expression Regulation, Neoplastic; D016147:Genes, Tumor Suppressor / Q000235:genetics; D015316:Genetic Therapy; D006801:Humans; D009062:Mouth Neoplasms / Q000235:genetics*; D009367:Neoplasm Staging; D017354:Point Mutation; D011506:Proteins / Q000502:physiology; D011519:Proto-Oncogenes / Q000235:genetics; D015398:Signal Transduction; D016211:Transforming Growth Factor alpha / Q000096:biosynthesis; D025521:Tumor Suppressor Proteins
D016588:Anticarcinogenic Agents; C096151:CDK2AP1 protein, human; D004273:DNA, Neoplasm; D011506:Proteins; D016211:Transforming Growth Factor alpha; D025521:Tumor Suppressor Proteins; D066246:ErbB Receptors