Background: Topoisomerase II-a is a molecular target of anthracyclines; several studies have suggested that topoisomerase II-a expression is related to response to anthracycline treatment. The objective of this study was to evaluate whether topoisomerase II-a overexpression predicts response to anthracycline treatment in locally advanced breast cancer patients. Methods: This prospective study included 50 patients with primary non-metastatic locally advanced breast cancer according to American Joint Committee for Cancer Staging(T3-4;N0-3) treated between January 2012 and Jaune 2012 at Clinical Oncology Department, Tanta University Hospital. Topoisomerase II-a, HER2, estrogen receptor (ER), progesterone receptor (PR) expression and KI-67 were evaluated by immunohistochemistry in formalin-fixed, paraffin-embedded breast tumors from 50 patients presenting with locally advanced breast cancer. Results: Tumors from 50 patients, 45 (90%) showed topoisomerase II-a overexpression, patients 34 (68%) for ER positive, 32 (64%) for PR positive, and 10 (20%) for HER2 overexpression and 16 (32%) for high KI 67. Significant correlation between clinical and pathological response was observed with topo IIA, HER2 and KI-67: p values of 0.001, 0.005 and 0.015, respectively. 1. Responders: Clinical CR: 3 patients had co-expression of topo II and HER2, hormonal receptor negative and high KI-67. Clinical PR: 43 patients majority of them had topo IIA overexpression .fig(9-10) 2. Non responders: 4 (8%) patients all had negative (TOPOII/HER2), low KI-67 and 2 were hormone receptor positive, and another 2 were hormone receptor negative. Conclusions: Our data support a correlation between topoisomerase II-a expression in locally advanced breast cancer patients and improved clinical benefit with neoadjuvant anthracycline-based therapy.
CITATION STYLE
Gamea, M. (2018). PO-468 The role of topoisomerase II-α (TOPO IIA) as a predictive factor for response to neoadjuvant anthracyclines based chemotherapy in locally advanced breast cancer. ESMO Open, 3, A206. https://doi.org/10.1136/esmoopen-2018-eacr25.488
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