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Prognostic Effect of Epithelial Cell Adhesion Molecule Overexpression in Untreated Node-Negative Breast Cancer
Purpose: Epithelial cell adhesion molecule (Ep-CAM) recently received increased attention not only as a prognostic factor in breast cancer but also as a potential target for immunotherapy. We examined Ep-CAM expression in 402 consecutive node-negative breast cancer patients with long-term follow-up...
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Published in: | Clinical cancer research 2008-09, Vol.14 (18), p.5849-5855 |
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Main Authors: | , , , , , , , , , , , , , , , , |
Format: | Article |
Language: | English |
Subjects: | |
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Online Access: | Get full text |
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Summary: | Purpose: Epithelial cell adhesion molecule (Ep-CAM) recently received increased attention not only as a prognostic factor in breast
cancer but also as a potential target for immunotherapy. We examined Ep-CAM expression in 402 consecutive node-negative breast
cancer patients with long-term follow-up not treated in the adjuvant setting.
Experimental Design: Ep-CAM expression was evaluated by immunostaining. Its prognostic effect was estimated relative to overexpression/amplification
of HER-2, histologic grade, tumor size, age, and hormone receptor expression.
Results: Ep-CAM status was positive in 106 (26.4%) patients. In multivariate analysis, Ep-CAM status was associated with disease-free
survival independent of age, pT stage, histologic grade, estrogen receptor (ER), progesterone receptor (PR), as well as HER2
status ( P = 0.028; hazard ratio, 1.60; 95% confidence interval, 1.05-2.44). Recently, so-called triple-negative (HER-2, ER, and PR)
breast cancer has received increased attention. We noticed a similar association of Ep-CAM with disease-free survival in the
triple-negative group as for the entire cohort.
Conclusion: In this study of untreated breast cancer patients, Ep-CAM overexpression was associated with poor survival in the entire
cohort and in the subgroup of triple-negative breast cancer. This suggests that Ep-CAM may be a well-suited target for specific
therapies particularly in HER-2–, ER-, and PR-negative tumors. |
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ISSN: | 1078-0432 1557-3265 |
DOI: | 10.1158/1078-0432.CCR-08-0669 |