39P - Evaluation of soluble E-Cadherin as a predictive marker for response to preoperative systemic chemotherapy in early breast cancer

Date 08 May 2014
Event IMPAKT 2014
Session Welcome reception and Poster Walk
Topics Breast Cancer, Early Stage
Translational Research
Presenter Christoph Suppan
Citation Annals of Oncology (2014) 25 (suppl_1): i8-i16. 10.1093/annonc/mdu066
Authors C. Suppan1, G. Steger2, M. Balic1, N. Dandachi1, A. Lang3, B. Mlineritsch4, C. Fesl5, H. Samonigg1, M. Gnant6, T. Bauernhofer1
  • 1Department Of Medicine, Division Of Oncology, Medical University of Graz, 8036 - Graz/AT
  • 2Department Of Medicine I, Medical University of Vienna, Vienna/AT
  • 3Department Of Internal Medicine, LKH Feldkirch, Feldkirch/AT
  • 4Department Of Internal Medicine, Paracelsus University Hospital Salzburg, Salzburg/AT
  • 5Department Of Statistics, ABCSG, Vienna/AT
  • 6Department Of Surgery, Medical University of Vienna, Vienna/AT

Abstract

Background:

Recent studies demonstrated that elevated levels of soluble E-cadherin (sE-cadherin), a product of proteolytic cleavage of cell-surface E-cadherin, are associated with higher risk for metastatic disease and poor prognosis in various tumor types. In a retrospective analysis, we have recently shown a significant association between sE-cadherin levels and histopathological regression scores. ABCSG-24, a randomised phase III trial comparing pathological complete response (pCR) rates of early breast cancer following preoperative systemic chemotherapy (PST) with epirubicin-docetaxel (ED) +/- capecitabine (EDC) with the addition of trastuzumab in Her2-positive tumors, was the perfect opportunity to prospectively evaluate, if sE-cadherin is a predictive marker for response to PST in breast cancer patients.

Materials and methods:

In this prospective analysis, sera of 196 patients undergoing PST for six cycles every three weeks were collected before initiation of each cycle. Soluble E-cadherin measurement was done by using a commercially available quantitative sandwich enzyme immunoassay technique. Histopathological response in surgically removed specimens was evaluated using a modified Sinn regression score. In univariate and multivariate analyses, sE-cadherin was correlated with pCR to PST and clinico-pathological parameters.

Results:

The median level of sE-cadherin in the group of patients with pCR was 3864.08 ng/ml (range: 2265.73–6613.84), whereas the median level without pCR was 3738.76 ng/ml (range: 1752.04–10838.16). This difference was not statistically significant (p = 0.31). Furthermore there was no significant difference between the sE-cadherin levels in the two therapy arms (ED vs. EDC). Regarding to clinico-pathological parameters pretreatment sE-cadherin showed a significant correlation with menopausal status (p = 0.036) and tumor grade (p = 0.0093). Histopathological response was significantly associated with hormone receptor status (p < 0.0001) and Her2-neu-status (p = 0.032).

Conclusion:

Our findings do not support a predictive or prognostic value of sE-Cadherin in breast cancer patients undergoing PST.

Disclosure:

All authors have declared no conflicts of interest.