Statement: E-cadherin is a transmembrane glycoprotein that mediates epithelial cell-to-cell adhesion and plays an important role in maintaining epithelial stability. E-cadherin expression is greatly reduced in many types of human cancers including oral cancer. An epigenetic alteration in association with promoter hypermethylation is one important mechanism of E-cadherin gene silencing. Materials and Methods: In our previous immunohistochemical study, we evaluated the expression of E-cadherin by immunohistochemical staining of 50 oral squamous cell carcinomas and found that the expression of E-cadherin was reduced in 40/50 (80%) primary tumors and in 21/22 (95.5%) lymph nodes. To correlate E-cadherin expression and its mechanism of regulation, approximately 1000 cells from representative cancers were microdissected and used for methylation-specific PCR to analyze the status of CpG promoter hypermethylation of the E-cadherin gene. Method of Data Analysis: n/a Results: As a preliminary result, we found that the promoter region of E-cadherin was hypermethylated in one specimen of 20 primary oral cancers. Conclusion: Our findings showed that aberrant expression of E-cadherin was not strongly associated with promoter hypermethylation of E-cadherin. Further study is needed on tumor recurrences and nodal metastases.