Grant: Travel Awards - Institute Community Support

Although tobacco is considered to be a risk factor for oral cancer, there is a subset of non-smokers who develop oral cancer. A decrease in the numbers of smokers has resulted an increased proportion of cases occurring among non-smokers (NS). Lesions with oral epithelial dysplasia (OED) are at risk of progressing to oral cancer. There is a gap in the knowledge of the clinical and genetic characterization, and the risk of progression in this growing category. The aim of this study was to: 1) describe the molecular and clinical features of OED in NS as compared to smokers; and 2) compare progression rates and time to progression in NS and smokers with OED. Subjects with biopsy confirmed mild or moderate OED were accrued from the BC Oral Cancer Prediction Longitudinal Study. A validated genomic test was performed on biopsies to collect molecular information. Clinical lesion features and detailed smoking history were collected. Progression was considered to be advancement to severe dysplasia, carcinoma in situ, or squamous cell carcinoma. Out of 231 OED, 30% were NS related, based on self-reported smoking status. Although there were more smokers with OED than NS, a significantly higher proportion of NS with OED underwent malignant as compared to ever smokers (ES). Time to outcome was also faster in this group. Smokers were more likely to have OED at the floor of mouth, while OED was more likely to occur at the tongue or gingiva in NS. Molecular risk patterns were strongly associated with progression and were equally sensitive in both NS and ES subgroups. These findings suggest that progressive lesions in NS and ES have similar genetic underpinnings, and emphasize the need to consider molecular profiles in the management of OED. Treatment of high-risk lesions, should be considered, reducing the number of individuals with advanced stage disease. OED at low risk for progression, could be monitored in a clinic setting, sparing the health care system considerable cost.