Oral cancer is the sixth most common cancer worldwide with a high prevalence in South Asia. Cancer of oral cavity accounts for almost 3% of cancer cases in the world. The incidence varies widely reflecting geographic differences in exposure to risk factors. Several risk factors for development of oral cancer are now well known including smoking, drinking and consumption of smokeless tobacco products. Genetic predisposition to oral cancer has been found in certain cases but its components are not yet entirely clear. The recent rise in younger age groups and females seen in many countries is of particular concern. Treatment and management of complications, loco regional recurrence and further primary tumors result in high morbidity and mortality especially when the disease is advanced stage at initial diagnosis. Progress in cancer research has provided abundant new knowledge about cellular processes and molecular biology underlying oral carcinogenesis and tumour progression. The natural history of oral cancer seems to gradually evolve through transitional precursor lesions from normal epithelium to a full-blown metastatic phenotype. A number of genomic lesions accompany this transformation and a wealth of related results has appeared in recent literature and is being summarized here. Furthermore, several key genes have been implicated especially well-known tumor suppressors like the cyclin dependent kinase inhibitors, TP53 and oncogenes like the cyclin family, EGFR. Viral infections, particularly with oncogenic HPV subtypes and EBV can have a tumorigenic effect on oral epithelia and their role is discussed along with potential therapeutic interventions. The present review attempts to summarize the current most widely-used research approaches and their application in the prevention, diagnosis, effective treatment, and improved outcome of oral cancer.
