Abstract:In the treatment of human epidermal growth factor receptor 2 (Her-2) overexpressing breast cancer, some patients have drug resistance to trastuzumab. Potential mechanisms of resistance to trastuzumab include impaired access of trastuzumab to Her-2; alternative signaling from insulin-like growth factor-1 receptor (IGF-1R), hepatocyte growth factor receptor (HGFR) and so on; aberrant downstream signaling caused by loss of phosphatase and tensin homologs deleted from chromosome 10 (PTEN); phosphatidylinositol 3-kinase catalytic alpha polypeptide gene (PIK3CA) mutation; over-expression of heat shock protein 90 (HSP90) and CD44. Additionally, potential strategies for overcoming resistance to trastuzumab include using new targeted medicines, such as pertuzumab, lapatinib and trastuzumab-DM1.

Key words:Breast neoplasms,Drug resistance, neoplasm,Trastuzumab,Molecular targeted therapy