Differential expression of e-cadherin in primary breast cancer and corresponding lymph node metastases

Abstract

Background/aim: E-Cadherin is a marker with a controversial function. Its role is often interpreted in the context of the epithelial-mesenchymal transition. In ambiguous cases, it is used as a phenotypic marker of lobular subtype of breast carcinoma. It has been well-studied in primary cancer, but its expression after metastasis is not well-described. The aim of this study was to determine the evolution of E-cadherin expression in no special type (NST) primary breast carcinoma and to correlate this with that in distant, paired nodal metastases (LNM) and molecular classification.

Material and methods: We processed 88 invasive breast carcinomas of NST type and their paired LNM. The specimens were formalin-fixed and paraffin embedded. Sections were immunostained for estrogen receptor (ER), progesterone receptor (PR), human epidermal growth factor receptor 2 (Her2), basal cytokeratin CK5, nuclear protein Ki67 and E-cadherin with a Leica Bond-Max autostainer.

Results: The results obtained were grouped into four molecular subtypes: Luminal A, luminal B, HER2-overexpressing, and triple-negative/basal-like. We found that the frequency of E-cadherin expression was higher (95.45%) in primary sites than in LNM (72.73%). E-Cadherin from primary breast cancer correlated positively only with E-cadherin in LNM (p≤0.003). A single positive correlation of E-cadherin with ER (p≤0.007) LNM was found.

Conclusion: E-Cadherin expression is not stable during the metastatic process. Its expression in LNM is lower than in primary sites. E-Cadherin expression in primary sites positively correlates with E-cadherin from LNM.

Keywords: Molecular subtypes; breast cancer; invasive carcinoma NST type; metastasis.