ABSTRACT
Human epidermal growth factor receptor 2(Her-2),which is often over-expressed in 20%-25% of invasive breast cancer patients,is associated with an aggressive tumor phenotype and therefore,a reduced survival rate.As a widely clinically applied Her-2-targeted monoclonal antibody,herceptin,when combined with chemotherapy,significantly increases the survival time of patients without tumors.However,the majority of the cancers that initially respond positively to herceptin begin to counteract against the treatment within just 1 year.This study described several important and well-known mechanisms as well as the updates and advancement in this field.These mechanisms include over-activation of the P13K/AKT pathway,abnormal expression in the EGFR family and their ligands,the masking of the Her-2 receptor,herceptin,activation of PI3K/AKT via an alternative pathway,over-expression of Darpp-32 and t-Darpp.autophagy of tumor cells and over-expression of HSP27,and more.