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{2286,2490}. Ploidy studies of dysplastic leukoplakias showed that the great majority of aneuploid lesions developed SCC in the follow-up period, by contrast with 60% of tetraploid lesions and only about 3% of diploid lesions {2490}. No correlation was found between the degree of dysplasia and DNA ploidy. Similar studies on erythroplasias {2491} confirmed the high predictive potential of aneuploidy in identify ing cases which progressed to SCC. Non-dysplastic white patches have also been studied {11} and although there was a much lower incidence of malignant transformation, 80% of such cases were aneu-ploid.

LOH studies have been undertaken contrasting oral lesions which progressed to SCC or carcinoma in-situ during follow-up with corresponding lesions which did not progress. LOH on two chromosome arms, 3p and 9p seemed to be particularly important in predicting progression {2201}.

Fig. 4.15 A Moderate dysplasia. Drop shaped rete ridges, dysplasia extending to mid-third and moderate cytological changes B Severe dysplasia into upper third of epithelium with marked cytological change C Severe dysplasia into upper third of epithelium with prominent cytological change including abnormal mitoses. D Carcinoma in-situ. Abnormal cells seen throughout the full thickness of epithelium.

Fig. 4.15 A Moderate dysplasia. Drop shaped rete ridges, dysplasia extending to mid-third and moderate cytological changes B Severe dysplasia into upper third of epithelium with marked cytological change C Severe dysplasia into upper third of epithelium with prominent cytological change including abnormal mitoses. D Carcinoma in-situ. Abnormal cells seen throughout the full thickness of epithelium.

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