L D Rock1, M P Rosin2, L Zhang3, B Chan4, B Shariati5, D M Laronde4. 1. Department of Oral Biological and Medical Sciences, the University of British Columbia, 2199 Wesbrook Mall, Vancouver, BC V6T 1Z3, Canada; BC Oral Cancer Prevention Program, BC Cancer Agency, Vancouver, BC V5Z 1L3, Canada. Electronic address: leigha.rock@alumni.ubc.ca. 2. BC Oral Cancer Prevention Program, BC Cancer Agency, Vancouver, BC V5Z 1L3, Canada; Department of Biomedical Physiology and Kinesiology, Simon Fraser University, Burnaby, BC V5A 1S6, Canada. 3. Department of Oral Biological and Medical Sciences, the University of British Columbia, 2199 Wesbrook Mall, Vancouver, BC V6T 1Z3, Canada; BC Oral Cancer Prevention Program, BC Cancer Agency, Vancouver, BC V5Z 1L3, Canada; BC Oral Biopsy Service, Department of Laboratory Medicine and Pathology, Vancouver General Hospital, 910 West 10th Avenue, Vancouver, BC V5Z 1M9, Canada. 4. Department of Oral Biological and Medical Sciences, the University of British Columbia, 2199 Wesbrook Mall, Vancouver, BC V6T 1Z3, Canada; BC Oral Cancer Prevention Program, BC Cancer Agency, Vancouver, BC V5Z 1L3, Canada. 5. Department of Oral Biological and Medical Sciences, the University of British Columbia, 2199 Wesbrook Mall, Vancouver, BC V6T 1Z3, Canada.
Abstract
OBJECTIVES: Tobacco usage is the strongest risk factor in the development of oral squamous cell carcinoma (OSCC), which mandates careful screening for oral cancers in smokers. However, there are indications that oral potentially malignant lesions, such as oral epithelial dysplasia (OED), in non-smokers (NS) have a higher cancer risk than those in smokers. Without tobacco as an etiology, the development of these lesions in NS may suggest genetic susceptibility. The increasing incidence of OSCC in NS calls for a better understanding of the natural history of OED in NS as compared to that of smokers. MATERIALS AND METHODS: Patients from a population-based longitudinal study with more than 10 years of follow up were analyzed. Of the 455 patients with primary OED (233 mild and 212 moderate dysplasia), 139 were NS and 306 were smokers. Demographic and habit information, clinical information (lesion site, size and appearance; toluidine blue and fluorescent visualization), microsatellite analysis for loss of heterozygosity (LOH) and outcome (progression) were compared between the two groups. RESULTS AND CONCLUSIONS: The majority of patients with OED were smokers. Of these, more were males, non-Caucasians and heavy drinkers. A significantly higher number of OED in NS were in the tongue, whereas a significantly higher number of OED in smokers were in the floor of mouth (FOM). OED in NS showed a greater than 2-fold increase in cancer progression. Strikingly, OED located in the FOM in NS showed a 38-fold increase in cancer progression as compared to those in smokers.
OBJECTIVES:Tobacco usage is the strongest risk factor in the development of oral squamous cell carcinoma (OSCC), which mandates careful screening for oral cancers in smokers. However, there are indications that oral potentially malignant lesions, such as oral epithelial dysplasia (OED), in non-smokers (NS) have a higher cancer risk than those in smokers. Without tobacco as an etiology, the development of these lesions in NS may suggest genetic susceptibility. The increasing incidence of OSCC in NS calls for a better understanding of the natural history of OED in NS as compared to that of smokers. MATERIALS AND METHODS:Patients from a population-based longitudinal study with more than 10 years of follow up were analyzed. Of the 455 patients with primary OED (233 mild and 212 moderate dysplasia), 139 were NS and 306 were smokers. Demographic and habit information, clinical information (lesion site, size and appearance; toluidine blue and fluorescent visualization), microsatellite analysis for loss of heterozygosity (LOH) and outcome (progression) were compared between the two groups. RESULTS AND CONCLUSIONS: The majority of patients with OED were smokers. Of these, more were males, non-Caucasians and heavy drinkers. A significantly higher number of OED in NS were in the tongue, whereas a significantly higher number of OED in smokers were in the floor of mouth (FOM). OED in NS showed a greater than 2-fold increase in cancer progression. Strikingly, OED located in the FOM in NS showed a 38-fold increase in cancer progression as compared to those in smokers.
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