DISTINCT PATTERNS OF E-CADHERIN CPG ISLAND METHYLATION IN PAPILLARY, FOLLICULAR, HURTHLES CELL, AND POORLY DIFFERENTIATED HUMAN THYROID-CARCINOMA

Expression of the invasion/metastasis suppressor, E-cadherin, is dimin ished or lost in thyroid carcinomas. Yet, mutational inactivation of E -cadherin is rare. Herein, we show that this loss is associated with h ypermethylation of the E-cadherin 5' CpG island in a panel of human th yroid cancer cell lines. This aberrant methylation is evident in 83% o f papillary thyroid carcinoma, 11% of follicular thyroid carcinoma, 40 % of Hurthle's cell carcinoma, and 21% of poorly differentiated thyroi d carcinomas. Contrary to previous reports, the majority of these poor ly differentiated thyroid carcinomas express E-cadherin, but often wit hin the cytoplasm rather than at the cell surface. Together, our data indicate that the invasion/metastasis suppressor function of E-cadheri n is frequently compromised in human papillary, Hurthle's cell, and pe arly differentiated thyroid carcinoma by epigenetic and biochemical ev ents.