Abstract
Abstract Background: Predicting the risk of distant micrometastasis of NSCLC after complete surgical resection is a significant problem to solve, and useful molecular markers that can predict recurrence have not yet been identified. The epithelial to mesenchymal transition (EMT) is an important contributor to the invasion and metastasis of epithelial-derived cancer. However, there is currently no data about the EMT status in primary NSCLC and its clinical usefulness to predict the recurrence and disease free survival (DFS). In addition, an association between insulin-like growth factor 1 (IGF1) and EMT-related molecules was reported, therefore, we also analyzed the association between the expression of IGF1R and EMT-related molecules. Methods: Tumor specimens were collected from 182 consecutive patients who underwent a complete resection for lung adenocarcinoma from 2003 to 2007 in our department. We analyzed the expression levels of EMT-related molecules (E-cadherin, gamma catenin and vimentin) in the primary lung adenocarcinoma by immunohistochemisty. We also analyzed the association between the expression of IGF1R and EMT-related molecules in the primary lung adenocarcinoma by immunohistochemisty. Results: The positive expression of E-cadherin, gamma catenin and vimentin was identified in 94 (51.4%), 82 (40.4%) and 32 (17.5%) patients, respectively. Their expression was not correlated with recurrence or disease-free survival (DFS) according to the survival analysis. Positive expression of IGF1R was detected in 43 (23.6%) patients, and its expression was significantly associated with the expression of E-cadherin and gamma-catenin, but not with vimentin.Conclusions: The EMT status in the primary tumor of NSCLC does not predict the recurrence and disease free survival. However, there was a significant association between the expression of IGF1R and several EMT-related proteins in patients with lung adenocarcinoma. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 1148. doi:1538-7445.AM2012-1148
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