Oral cancer pathophysiology
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Simrat Sarai, M.D. [2]
Overview
Genes involved in the pathogenesis of oral cancer include tumor suppressor genes (TSGs), particularly in chromosomes 3, 9, 11, and 17.
Pathophysiology
The pathophysiology of oral cancer involves inactivated tumor suppressor genes, P16, and TP53 and overexpressed oncogenes, PRAD1.The molecular changes in oral squamous cell carcinoma in western countries (eg, United Kingdom, United States, Australia), are particularly TP53 mutations. These mutations are infrequent in eastern countries (eg, India, Southeast Asia), where the involvement of ras oncogenes is more common.
Pathology of Malignant tumors of oral cavity
Squamous cell carcinoma (SCC) tumours make up 95% of all oral cavity cancers. They are classified based on macroscopic or microscopic features. Macroscopic features of squamous cell carcinoma are: Infiltrative – Cancer is growing into the deeper layers of the oral cavity. Exophytic – Cancer is growing outwards from the surface of the oral cavity. Verrucous – Cancer has a wart-like appearance.U Ulcerated – Cancer appears as an open sore.F Flat – Cancer appears as an abnormal area in the lining of the oral cavity. Microscopic features can be seen only with a microscope:
- Type of cells.
Differentiation: The cancerous cells may be well differentiated (look like normal cells), moderately differentiated or poorly differentiated (do not look or act like normal cells).
- Keratinization: Keratin is a protein found in the hair, skin and some mucous membranes. It makes tissue tough.
- Keratinized SCC has more keratin in the tumour.
- Non-keratinized SCC has very little or no keratin in the tumour.
- Well-differentiated SCC is usually keratinized, while poorly differentiated SCC is non-keratinized.
- Invasion of the cancer into deeper layers and tissues, such as fat and muscle.