Abstract
Breast cancers over-express the human epidermal growth factor receptor 2 (HER2) in about 15% of patients. This transmembrane tyrosine kinase receptor activates downstream signaling pathways and leads to proliferation of cancer cells. Trastuzumab, an anti-HER2 monoclonal antibody, improves outcome in women with early and metastatic breast cancer. Resistance to trastuzumab involves the phosphoinositide 3-kinase/mammalian target of rapamycin (PI3K/mTOR) pathway, truncation of the Her2 receptor or lack of immune response. The last decade has seen major advances in strategies to overcome resistance to trastuzumab. This includes the development of antibody-drug conjugates, dual HER2 inhibition strategies, inhibition of PI3K/mTOR pathway and development of modulators of immune checkpoints.
Highlights
About 15% of breast cancer over-expresses the human epidermal growth factor receptor 2 (HER2) [1,2]
HER2 is a transmembrane tyrosine kinase receptor that is a member of the human epidermal growth factor receptor (EGFR/HER) family
In another randomized trial performed in the neoadjuvant setting (Neo ALTTO), patients were randomized among lapatinib, trastuzumab or lapatinib plus trastuzumab, all in combination with paclitaxel after six weeks of targeted therapy alone
Summary
About 15% of breast cancer over-expresses the human epidermal growth factor receptor 2 (HER2) [1,2]. It could prevent signaling related to truncated HER2 receptor or enhance trastuzumabdependant ADCC, thanks to an accumulation of HER2 at the cell surface It has shown its efficacy when combined with capecitabine, in terms of time to progression (hazard ratio (HR): 0.57; 95% confidence interval (CI) 0.43 to 0.77; P
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