Oral cancer in the molecular age.

Abstract

Oral cancer represents an accumulation of defects in the genes that encode key proteins associated with growth and development. Dysregulation of these proteins is central to malignant conversion. This appears to involve three major changes in cell function: 1. altered cell growth, death and longevity; 2. unencumbered cell movement; and 3. development of a new blood supply (angiogenesis). Specific genes, such as p53, p27, p16, and cyclin D-1, are altered in oral cancer through mutation, amplification, or deactivation. These genes are also frequently altered in many other malignancies. In oral mucosa, etiologic agents--especially tobacco and alcohol, and possibly some viruses--are known to induce alterations in the genes and gene functions associated with cell cycle regulation, contributing to the development of squamous cell carcinoma and epithelial dysplasias. Identification of the specific genes/proteins and the sequence in which they appear in the transformation of a normal cell to a malignant cell is necessary for the formulation of new treatment strategies, the development of early detection methods, and the prediction of patient outcome.