The annual San Antonio Breast Cancer Conference is always of interest, and the conference itself always lives up to expectations. The section on targeted therapy focused on the combination of targeted therapy and other treatment modalities, such as combination with chemotherapy and endocrine therapy, as well as multi-targeted combination, and various clinical trials were mainly reported; while the related basic research focused on the mechanism of action of targeted drug therapy, the molecular basis of resistance and sensitivity, and the fine regulation between different molecules in the related signaling pathways, the interaction between proteins. Among them, trastuzumab for Her-2 remains the focus, while lapatinib, pertuzumab and sunitinib and other vascular endothelial growth factor inhibitors, although not as heavily written, still show new therapeutic opportunities that are no longer comparable. 1, Her-2 treatment effective and resistance mechanism: Targeted therapy is developed with molecular biology technology, and human research in this field has experienced a long time until the anti-hormone receptor treatment, monoclonal antibodies and small molecule tyrosine kinase inhibitors appeared, but these treatments still have resistance problems in addition to bringing leaps and bounds of therapeutic progress, how to understand this phenomenon has become a further The 30th Annual Meeting was no exception. The Her-2 family has four surface receptors, Her-1-4, and 11 ligands, and signaling is finely regulated from the membrane to the nucleus, with a number of transcription factors in the outer layers, including the Her-2 gene amplification in the absence of a clear ligand. Trastuzumab targeting the Her-2 receptor has a single-agent efficiency of 30% in metastatic breast cancer and an adjuvant chemotherapy efficiency of 50%, and the mechanism of drug resistance can be understood at several levels: (1) incomplete signaling blockade: because other dimers of the Her-2 family can still be activated to transmit signals to make tumor cells grow, if all heterodimers can be completely Blocking all heterodimers is the only way to achieve complete inhibition, such as small molecule tyrosine kinase inhibitors: lapatinib, gefitinib, erlotinib, and currently some preclinical studies by the combination of the above drugs in order to block Her-2 and its family as much as possible; (2) trastuzumab works by binding to the outer part of the Her-2 cell membrane, and if the outer part of the membrane is missing, such as tumor cells express p95ErbB2, it cannot bind Her-2 receptor and thus cannot function. 9% of breast cancer p95ErbB2 is overexpressed; small molecule tyrosine kinase inhibitors such as lapatinib can enter the cell through the cell membrane and bind to the intracellular part of Her-2, so currently lapatinib can be used as an antidote treatment for the failure of trastuzumab treatment. 2. The role of ribosome (polysomy) 17 in the Her-2 positive adjuvant trastuzumab treatment trial in the N9831 clinical trial: The Her-2 gene is localized on human chromosome 17q21. Recently, it was initially found that an abnormal number of chromosome 17, ribosome 17 amplified (p17) or normal (n17), was associated with the efficacy of trastuzumab in the treatment of metastatic breast cancer, and this The study was designed to determine the prognosis of Her-2 gene replication and chromosome 17 status with or without trastuzumab in patients enrolled in 1888 patients from the Her-2 positive N9831 adjuvant trastuzumab phase III clinical trial, with the initial study endpoint of observing DFS and detecting Her-2 in the Mayo clinical laboratory using the FISH method. The interesting finding was that patients not treated with trastuzumab had a 34% lower DFS with p17 than with n17, p=0,04; in the group treated with trastuzumab, both p17 and n17 improved DFS with risk ratios of 0,52 (p=0,006) and 0,37 (p=0,0004), respectively, concluding that for standard chemotherapy there was a greater benefit in patients with p17 than with n17 , whereas if trastuzumab was added either 3 or 5 years of disease-free survival was not affected. 3. whether there is a difference between her-2 immunohistochemistry and central laboratory FISH in different regions: this study provides some evidence for this in the recently published ASCO guidelines for the use of IHC and FISF to determine HER-2 gene amplification or protein expression to guide treatment with trastuzumab. the DFS was compared with her-2 immunohistochemistry and central laboratory FISH done in different regions. Comparison of FISH from the HERA (BIG01-01) trial. In the HERA trial patients with tissues for IHC3+ and 2+ were sent to the central laboratory for retesting and were only selected for inclusion if the central laboratory IHC3+ or FISH+. Patients randomized in the HERA trial with trastuzumab for one year and observation were analyzed with a median follow-up of 23, 5 M. The 3-year DFS was 80, 4% in the trastuzumab group (n=1703) and 74, 4% in the observation group (n = 1698) risk ratio 0, 64, Conclusion: local area IHC testing and central laboratory HER-2(+) did not show a difference in the HERA trial after completion of adjuvant chemotherapy in both the 1 year trastuzumab treatment and observation groups, but the results of the NCCTG9831 subgroup analysis suggest a lack of clinical benefit with trastuzumab in the IHC 2+/FISH+ subgroup.