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Department of Surgery II, Osaka University Medical School, 1-1-50 Fukushima-ku, Osaka 553 Japan [H. O., H. S., M. I., H. T., T. K., T. M.]; Department of Surgery, National Osaka Hospital, Osaka 553, Japan [Y. T., K. K.]; and Department of Biophysics, Faculty of Science, Kyoto University, Kyoto, Japan [N. M., S. H., M. T.].
E-cadherin (E-cad) is a subclass of the cadherin family that plays a major role in maintenance of intercellular junctions in epithelial tissues. In order to explore the correlation between the expression of E-cad and cancer invasion and metastasis in vivo, we performed an immunohistochemical examination for E-cad expression in 120 patients with breast cancer using our specific anti-E-cad monoclonal antibody.
In noncancerous epithelial cells, E-cad was strongly expressed on cell-cell boundaries, whereas various staining patterns were observed in tumors. Of these 120 tumors, 56 (47%) showed Pr type expression of E-cad, and 64 (53%) showed Rd type or negative expression. We found significant correlations between E-cad expression and clinicopathological features. The frequency of Rd type was significantly higher in invasive ductal carcinomas (58%, 56 of 97) and poorly differentiated carcinomas (84%, 21 of 25) than in noninvasive and well-differentiated carcinomas.
Furthermore, a high frequency of Rd type was detected in the following advanced tumors: T3,4 tumors, 71% (22 of 31); tumors with extensive lymph node metastasis, 74% (29 of 39); and tumors with distant metastasis, 86% (19 of 22). These values were significantly higher compared with their counterparts.
The expression of epidermal growth factor receptor tended to be positive in E-cad-positive tumors. However, no significant relationship was seen among E-cad expression, menopausal status, hormone receptor status, and DNA ploidy pattern. These results suggest that the reduction of E-cad expression may play an important role in invasion and metastasis of human breast cancer.
1 This work was supported in part by a Grant-in-Aid for Cancer Research (04454333) from the Ministry of Education, Science and Culture of Japan.
2 To whom requests for reprints should be addressed.
Received 9/ 3/92. Accepted 1/21/93.
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