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British Columbia Cancer Research Centre, Vancouver, British Columbia, V5Z 1L3 [M. P. R., W. L. L., N. D. L.]; School of Kinesiology, Simon Fraser University, Burnaby, British Columbia, V5A 1S6 [M. P. R., C. P., R. J. L., T. Z.]; and Faculty of Dentistry, the University of British Columbia, Vancouver, British Columbia, V6T 1Z3 [C. P., R. P., L. Z.] Canada
Treatment induces reactive changes that often resemble low-grade dysplasia at former oralcancer sites, complicating histopathological assessment. We tested a set ofmicrosatellite markers shown previously to be predictive of progression for oral premalignant lesions for the ability to predict development of second oral malignancy (SOM). Sixty-eight oral leukoplakia at former cancer sites (with known outcome, 36 progressed to SOM) were evaluated for loss of heterozygosity at 19 loci on seven chromosome arms. 3p and/or 9p loss in these posttreatment leukoplakia was associated with a 26.3-fold increase in risk of developing SOM compared with those that retained both of these arms (P < 0.001), with 60% of cases with loss of heterozygosity developing SOM in 2 years. In contrast, histological diagnosis (moderate or severe dysplasia versus hyperplasia or mild dysplasia) had only a 1.7-fold increase in risk (P = 0.11). The identification of 3p and 9p loss in posttreatment lesions could serve as a simple and direct test for stratifying risk of SOM development.
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