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Updated: May 7, 2025

Optimization of a Multiplex RNA-based Expression Assay Using Breast Cancer Archival Material
Published on: August 1, 2018
Possibility of Human Epidermal Growth Factor Receptor 2 Expression as a Treatment Selection Indicator in Early
Namiko Tanaka1, Seiichi Imanishi1, Chisato Takeuchi1
1Department of Breast Surgery, Osaka Rosai Hospital, Osaka, JPN.
Abstract:
Background This study aimed to evaluate the relationship among human epidermal growth factor receptor 2 (HER2) expression level, pathological complete response (pCR) rate of neoadjuvant chemotherapy, and prognosis in early-stage triple-negative breast cancer (TNBC). Methodology This retrospective study analyzed the relationship among HER2 expression level, pCR rate, clinicopathological factors, and prognosis in 39 patients who were diagnosed with TNBC between 2012 and 2020 at Osaka Rosai Hospital and underwent surgery after neoadjuvant chemotherapy (NAC). Results Patients' age ranged 33-86 (median = 57) years, and the observation period ranged 5-130 (median = 60) months. The HER2 expression levels were HER2 (0), HER2 (1+), and HER2 (2+, fluorescence in situ hybridization test (FISH); negative) for 18, 12, and 9 cases, respectively. The pCR rates were 38.9%, 8.3%, and 44.4% for HER2 (0), HER2 (1+), and HER2 (2+, FISH; negative), respectively, and no correlation was observed with the degree of HER2 expression. The prognosis of distant disease-free survival (DDFS) differed depending on the HER2 status (p = 0.032), and this trend was also observed in overall survival (OS) (p = 0.012). This tendency became even stronger when comparing HER2-low and HER2 (0) (p = 0.028 and p = 0.01, respectively). HER2 expression was significantly decreased from before to after NAC (p = 0.001). Conclusions HER2 expression did not correlate with the pCR rate of NAC but did correlate with DDFS and OS. Thus, patients with an HER2 (0) status are considered to have a poor prognosis and should be more aggressively considered for perioperative chemotherapy, e.g., immune checkpoint inhibitors.
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