Oral cancer pathophysiology
|
Oral cancer Microchapters |
|
Diagnosis |
|---|
|
Treatment |
|
Case Studies |
|
Oral cancer pathophysiology On the Web |
|
American Roentgen Ray Society Images of Oral cancer pathophysiology |
|
Risk calculators and risk factors for Oral cancer pathophysiology |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];{{AE}] Simrat Sarai, M.D. [2]
Overview
Pathophysiology
Oral carcinogenesis like any other cancer is a progressive disease and normal epithelium passes through stages starting from dysplasia to finally transforming into invasive phenotypes. Although all types of carcinomas are seen in oral cavity, the most common form of Oral carcinogenesis is squamous cell carcinoma. Use of genetic and proteomic approach in recent years have revealed the molecular pathological picture of oral carcinogenesis There is active search to identify genetic alterations in oncogenes or tumour suppressor genes, role of genomic instability and epigenetic modifications and to generate a gene expression profile in oral oncogenesis [20]. Understanding these genetic changes and gene expression patterns are keys to the understanding of molecular pathogenesis of OC. Though, there are some significant leads achieved, the complete understanding of molecular pathology of OC and its association with causative agent will require another decade of intensive research. We have discussed some of the important updates in this area of active research. Genetic Susceptibility
It is now established that up to 10% of all cancers have a strong hereditary component. Role of genetic component in the development of OC is being suggested by several studies showing familial clustering [21]. A clustering of OC has been seen in certain ethnic groups, like Askenazi group in Israel; with incidence being double as compared to other Jewish population in that country. However, the basis of this genetic susceptibility is not well understood, as yet.
Evaluation of specific genetic polymorphism in key genes involved in oral carcinogenesis has been the major area of study. Glutathione S-transferase M1 (GSTM1) null genotype appears to be the most consistent polymorphic susceptibility marker for head and neck cancer including OC. Meta-analyses by Tripathy and Roy showed that the GSTM1 null genotype conferred a 20–50% significantly increased HNSCC risk [22].
The variant val allele of the CYP1A1 (Cytochrome P450, family 1, member A1) polymorphism is another fairly consistent susceptibility marker with a 35% increased risk in a meta- analysis of 12 studies [21]. The studies on many other gene polymorphisms have been inconclusive. Brennan et al. [23] found that ALDH1B and ALDH2 (Aldehyde dehydrogenase 2) genes were associated with HNSCC and showed significant correlation with alcohol consumption.