Immunohistochemical determination and grading of CerbB-2 expression in breast cancer: correlation with interpectoral, apical nodal involvement and other prognostic factors

Abstract

We aimed to investigate the correlation between quantitative CerbB-2 expressions with conventional prognostic factors, and distinct nodal involvement in patients with invasive breast carcinoma. One hundred fifty seven consecutive breast carcinoma patients were retrospectively analysed. Level I-II, Level III, and Rotter (Interpectoral) group lymph nodes were separately examined and recorded. For each patient estrogen receptor (ER), progesteron receptor (PR), CerbB-2, P53 status were defined using immunohistochemistry. Age, tumor localisation, menopausal status, grade and the presence of intraductal component were also recorded. CerbB-2 expression did not correlate with age, localisation and menopausal status. There was a reverse, but weak correlation with tumor size and CerbB-2 expression (p=0.034). In subgroup analysis of CerbB-2 positive cases, the magnitude of CerbB-2 positivity did not correlate with tumor size (p=0.551). In univariate analysis CerbB-2 expression did not correlate with nodal involvement in Level I-II, and Rotter. In subgroup analysis of patients with positive CerbB-2, positivity of CerbB-2 linearly increased with the number of positive lymph nodes in Level I-II, and this difference was significant (p=0,039). There was a significant correlation between CerbB-2 expression and Level III nodal metastases (p=0.005). But this correlation was not significant among CerbB-2 positive patients (p=0.82). P53, PR positivity and the presence of intraductal component did not differ according to oncogene expression. We detected a reverse correlation with ER positivity and CerbB-2 positivity (p=0.011). It is concluded that quantitative expression of CerbB2 positivity increases with nodal involvement in Level I-II axillary lymph nodes, and ER. Also, CerbB-2 positivity is more common among patients with Level III lymph node metastases. (c) Versita Warsaw and Springer-Verlag Berlin Heidelberg. All rights reserved.