Oral cancer refer to any cancerous tissue growth located in the mouth. It may arise as a primary lesion originating in any of the oral tissues, by metastasis from a distant site of origin, or by extension from a neighboring anatomic structure, such as the nasal cavity or the maxillary sinus. As the most common form of oral cancer, squamous cell carcinoma (OSCC) usually involves the tissue of the lips or the tongue. The clinical natural history of OSCC development usually involves normal oral mucosa changing to oral leukoplakia (or IEN) changing to OSCC. Illustrated by molecular progression models, oral IEN is a pathologically discernable intermediate state between normal epithelium and invasive cancer . Clinically relevant IEN has genetic or epigenetic alterations, loss of cellular control, phenotypic characteristics overlapping those of invasive cancer.

Molecular (genetic and epigenetic) progression model of multistep oral carcinogenesis. The white central steps of the figure represent the progression of oral intraepithelial neoplasia from leukoplakia (white patches) to erythroplakia (red patches), which can precede cancer. This process involves activation of the epidermal growth factor receptor (EGFR) and related downstream events (eg, involving cyclooxygenase-2 [COX-2] and cyclin D1) leading to dysregulated proliferation, increasing frequency of mutations causing genomic instability (and vice versa) and invasion. LOH, loss of heterozygosity; RAR-ß, retinoic acid receptor-beta.