Abstract 146P
Background
The prognostic role of human epidermal growth factor receptor 2 (HER2) low expression in estrogen receptor (ER)-positive, HER2-negative breast cancer is not well described. The aim of this study is to compare disease characteristics and outcomes between HER2-low to HER2-0, in early-stage luminal disease.
Methods
A single center retrospective study comprising all women with ER-positive, HER2-negative early breast cancer, for whom an Oncotype DX test was performed between 2005-2012. Women were grouped to HER2-low (immunohistochemistry +1 or +2 and in situ hybridization not amplified) or HER2-0. Clinico-pathological features including tumor size, nodal involvement, grade, ki-67, intensity of hormone receptors expression, histology subtype lympho-vascular and perineural invasion and Oncotype recurrence score (RS) were collected. Data on overall survival (OS), disease-free survival (DFS) and distant DFS (DDFS) were also evaluated. Differences by HER2 expression were investigated.
Results
608 women were included, of which 304 women had HER2-0 and 304 had HER2-low disease. Lobular subtype was more common in HER-0 compared to HER2-low disease (17% vs. 8%, p=0.005). All other characteristics did not differ between the two groups. At a median follow up of 10.3 years, OS, DFS and DDFS were similar for the whole population. Analyses by genomic risk showed comparable outcomes for women with low genomic risk (RS≤25), but for women with high genomic risk (RS>25), HER2-low was associated with significantly favorable OS (HR=0.31, 95% CI 0.11-0.78, p=0.01), DFS (HR= 0.40, 95% CI 0.20-0.82; p=0.01) and DDFS (HR=0.26, 95% CI 0.11-0.63, P=0.002).
Conclusions
The prognostic impact of HER2-low expression in early-stage luminal disease varies across the genomic risk, with significant favorable outcomes of HER2-low compared to HER2-0 in women with high genomic risk. As other prognostic characteristics were comparable between HER2-low and HER2-0, our findings may be consistent with a novel prognostic feature for this population.
Clinical trial identification
Editorial acknowledgement
Legal entity responsible for the study
The authors.
Funding
Has not received any funding.
Disclosure
A. Moore: Other, Personal, Other, honorarium: Merck; Other, Personal, Other, honorarium: Roche. M. Sarfaty: Other, Personal, Advisory Board: Merck; Other, Personal, Advisory Board: Novartis; Other, Personal, Advisory Board: Roche. S. Stemmer: Other, Personal, Research Grant: Teva; Other, Personal, Research Grant: Clovis Oncology; Other, Personal, Research Grant: AstraZeneca; Other, Personal, Research Grant: BioPharma; Other, Personal, Research Grant: Puma Biotechnology; Other, Personal, Research Grant: Lilly; Other, Personal, Research Grant: Bristol Myers Squibb; Other, Personal, Research Grant: Roche; Other, Personal, Research Grant: MSD; Other, Personal, Research Grant: Moderna Therapeutics; Other, Personal, Research Grant: Exelixis; Other, Personal, Research Grant: Rafael Pharmaceuticals; Other, Personal, Research Grant: CTG Pharma; Other, Personal, Research Grant: Syncore; Other, Personal, Research Grant: Can-Fite BioPharma. R. Yerushlami: Other, Personal, Invited Speaker: Roche; Other, Personal, Invited Speaker: Teva; Other, Personal, Invited Speaker: MSD; Other, Personal, Invited Speaker: AstraZeneca; Other, Personal, Invited Speaker: Novartis; Other, Personal, Invited Speaker: Medison; Other, Personal, Advisory Role: Pfizer . H. Goldvaser: Other, Personal, Other, honorarium: Roche; Other, Personal, Other, honorarium: Pfizer; Other, Personal, Invited Speaker, honorarium: Novartis; Other, Personal, Other, honorarium: Oncotest. All other authors have declared no conflicts of interest.