RESUMO
Dysregulation of oncogenes, overproduction of growth factor receptors and their ligands, and loss of function of tumor suppressor genes are thought to contribute to multi-step process of carcinogenesis. It is suggested that proliferation markers like epidermal growth factor receptor (EGFR) actively participate in oral carcinogenesis, during initiation or promotion stage of the process. Potent mitogens such as epidermal growth factor (EGF) and transforming growth factor-alpha (TGF-a) mediate their growth responses through the common transmembrane glycoprotein receptor, EGFR. Current data suggest that a good number of epithelial cancers including oral squamous cell carcinomas (OSCC) overexpress EGFR and that monoclonal antibodies directed against EGFR may provide valuable information that would be useful in planning proper palliative treatment of certain premalignant and malignant lesions derived from squamous epithelium.