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자료유형
학술저널
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저널정보
대한병리학회 Journal of Pathology and Translational Medicine Journal of Pathology and Translational Medicine 제39권 제3호
발행연도
2005.1
수록면
187 - 191 (5page)

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Background : E-cadherin is a transmembrane glycoprotein, which has been shown to mediate calcium-dependent epithelial cell adhesion. A loss of E-cadherin expression has been associated with the tumor invasion and metastatic potential in some human cancers. The objective of this study was to evaluate E-cadherin expression in T1 breast ductal carcinomas in order to determine whether the loss of E-cadherin expression is correlated with lymph node metastasis. Methods : One hundred seventy nine patients with breast invasive ductal carcinoma, measuring less than 2 cm, were enrolled in this study. The subjects were divided into two groups on the basis of the status of the ipsilateral axillary lymph node, T1N1 (lymph node positive, n=91) or T1N0 (lymph node negative, n=88). None of the patients in this study had undergone preoperative chemotherapy. Formalin-fixed paraffin-embedded tissue sections of the primary breast cancers were stained by immunohistochemistry, using a mouse monoclonal antibody against E-cadherin. E-cadherin expression was designated as either positive (complete membranous staining) or negative (absent or incomplete membranous staining). Results : Benign breast parenchyma adjacent to invasive carcinoma was positive for E-cadherin. The loss of E-cadherin expression in the tumor was observed in 42% of patients of the T1N1 group, and in 24% of the T1N0 group. There was a significant correlation between the loss of E-cadherin expression and lymph node metastasis in the examined breast invasive ductal carcinomas (p=0.011). Conclusions : Our findings suggest that E-cadherin is an important molecule with regard to both tumor cell adhesion and metastasis, and its absence may constitue an early event in metastatic development. Therefore, E-cadherin may be a useful predictive marker for nodal metastasis in patients suffering from invasive ductal carcinoma.

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