Axillary response according to neoadjuvant single or dual human epidermal growth factor receptor 2 (HER2) blockade in clinically node‐positive, HER2‐positive breast cancer

Abstract

Incorporating dual human epidermal growth factor receptor 2 (HER2) blockade into neoadjuvant systemic therapy (NST) led to higher response in patients with HER2‐positive breast cancer. However, axillary response to treatment regimens, including single or dual HER2 blockade, in patients with clinically node‐positive breast cancer remains uncertain. Our study aimed to examine the pathologic axillary response according to the type of NST, that is, single or dual HER2 blockade. In our study, 546 patients with clinically node‐positive, HER2‐positive breast cancer who received NST followed by axillary surgery were retrospectively selected and divided into three groups: chemotherapy alone, chemotherapy\u2009+\u2009trastuzumab and chemotherapy\u2009+\u2009trastuzumab with pertuzumab. The primary outcome was the axillary pathologic complete response (pCR). Among 471 patients undergoing axillary lymph node dissection, the axillary pCR rates were 43.5%, 74.5% and 68.8% in patients who received chemotherapy alone, chemotherapy\u2009+\u2009trastuzumab and chemotherapy\u2009+\u2009trastuzumab with pertuzumab, respectively. There was no difference in axillary pCR rates between patients who received single or dual HER2 blockade (P = .379). Among patients receiving chemotherapy\u2009+\u2009trastuzumab, patients without breast pCR had the greatest risk for residual axillary metastases (relative risk, 9.8; 95% confidence interval, 3.2‐14.9; P\u2009<\u2009.0001). In conclusion, adding trastuzumab to chemotherapy increased the axillary pCR rate in patients with clinically node‐positive, HER2‐positive breast cancer; furthermore, dual HER2‐blockade with trastuzumab and pertuzumab did not elevate the axillary response compared with trastuzumab alone. Breast pCR could be a strong predictor for axillary pCR in clinically node‐positive patients treated with HER2‐targeting therapy.