Triple negative breast cancer (TNBC), which is a breast cancer with negative expression of estrogen receptor (ER), progesterone receptor (PR) and HER-2, is considered as an independent clinicopathological type with aggressive and poor prognosis, accounting for 10%-20% of all breast cancers. For metastatic triple-negative breast cancer, the main treatment modality is still chemotherapy due to the lack of endocrine therapy and anti-HER2 targeted therapy, while some patients may choose anti-angiogenic targeted therapy. Due to the few treatment options and poor prognosis, triple-negative breast cancer remains a difficult and hot research area in the field of breast cancer treatment. There is no reliable evidence to confirm that triple negative breast cancer is sensitive to specific chemotherapeutic agents, so current guidelines still recommend chemotherapy with anthracyclines and paclitaxel for triple negative breast cancer that has not received chemotherapy before. Some patients with triple-negative breast cancer may benefit more from platinum-based chemotherapy The mechanism of action of platinum-based drugs is through direct binding to DNA, causing intra- or interstrand cross-linking, which leads to the dissociation of double-stranded DNA, triggering cell growth arrest and possibly inducing cell death. During DNA double-strand damage repair, both require a homologous recombination repair process involving BRCA1 and BRCA2 proteins; therefore, mutations in either BRCA1 or BRCA2 will result in malfunctioning homologous recombination repair. One of the characteristics of cells with BRCA1 or BRCA2 mutations is their sensitivity to DNA cross-linking drugs.Patients with BRCA-mutated breast cancer have a higher proportion of triple-negative breast cancers than those with all disseminated breast cancers Some studies are currently exploring the role of platinum-based drugs in the treatment of metastatic triple-negative breast cancers in BRCA-mutated breast cancers.The 2014 San Antonio Breast Cancer Conference ( SABCS) reported on a clinical study of carboplatin versus docetaxel in first-line treatment of advanced triple-negative breast cancer or BRCA1/2-mutated breast cancer (TNT study). The results showed that in unselected triple-negative breast cancer, the primary observed endpoint (objective efficiency) and the secondary observed endpoint (time to disease progression-free) were similar for both drugs, with no significant differences. In contrast, the study in 43 patients with BRCA mutations showed that the objective efficiency rate was significantly higher in the carboplatin-treated group than in the docetaxel-treated group. This study suggests that carboplatin is not superior to docetaxel in unselected triple-negative breast cancer, but there is a significant advantage of carboplatin treatment in patients with BRCA1/2 mutations. Whether platinum-based chemotherapy regimens can be preferred in triple-negative breast cancer without BRCA testing remains controversial In March 2015 Chinese scholars reported in the journal LancetOncology the results of the CBCSG006 trial, a randomized, controlled, phase III clinical study comparing a cisplatin + gemcitabine regimen with a paclitaxel + gemcitabine regimen for the first-line treatment of metastatic triple-negative breast cancer. This is a randomized, controlled, phase III clinical study comparing cisplatin + gemcitabine regimen with paclitaxel + gemcitabine regimen for the first-line treatment of metastatic triple negative breast cancer. A total of 240 patients with recurrent primary triple-negative breast cancer were enrolled, most of whom had been treated with anthracyclines (>80%) and/or paclitaxel (>60%) during the (neo)adjuvant phase. The results showed that the PFS cisplatin + gemcitabine group was significantly better than the paclitaxel + gemcitabine group. The study suggests that first-line chemotherapy may be preferable to cisplatin in combination with gemcitabine for triple-negative breast cancer, especially for patients who have been treated with anthracyclines and paclitaxel in the adjuvant phase. The results of three phase III clinical trials, E2100, AVADO and RIBBON-1, have established the importance of bevacizumab in the treatment of metastatic breast cancer. The results of these three studies showed that bevacizumab + chemotherapy (paclitaxel, docetaxel, anthracyclines, capecitabine) was significantly better than chemotherapy alone in terms of PFS. Meta-analysis of 621 of these triple-negative breast cancers showed that bevacizumab in combination with chemotherapy significantly prolonged PFS, but in terms of OS, bevacizumab still did not show an advantage in triple-negative breast cancers. The TANIA study, a randomized, controlled, phase III clinical trial, showed a significant median prolongation in the bevacizumab+chemotherapy group compared to the chemotherapy-only group in patients who benefited from first-line bevacizumab in combination with chemotherapy, but the overall survival data were not yet mature. Although the results of the study are promising, whether long-term, ongoing bevacizumab treatment is justified in terms of economic aspects and adverse effects remains controversial. Some other small molecule tyrosine kinase inhibitors with anti-angiogenic effects, such as sorafenib and sunitinib, have also shown partial efficacy in clinical studies, but further validation in large-scale clinical trials is needed. In clinical practice, bevacizumab in combination with chemotherapy can be considered for some triple-negative breast cancer patients, especially those with heavy tumor load and rapid disease progression. PARP inhibitors need to be explored In BRCA-deficient cells, the impaired homologous recombination repair pathway makes other DNA repair pathways more important. Poly(adenosine diphosphate ribose polymerase-1) (PARP1), a key enzyme for DNA single-strand break repair, is more sensitive to breast cancer patients with BRCA 1/2 mutations. The results of the phase II clinical study of Iniparib in triple-negative breast cancer presented at the 2009 ASCO Annual Meeting were encouraging, as Iniparib in combination with gemcitabine/carboplatin significantly prolonged PFS and OS in patients with triple-negative metastatic breast cancer. PFS and OS, but the same results were not obtained in the Phase III clinical study. A randomized, controlled, phase III clinical study evaluating Olaparib versus physician-selected chemotherapy regimens for the treatment of BRCA1/2 mutated metastatic breast cancer is currently underway (D0819C00003). 310 patients with HER2-negative and BRCA1/2-mutated breast cancer, including triple-negative breast cancer, are planned to be enrolled. The final results of this study may provide a new therapeutic strategy for the treatment of triple-negative breast cancer. PD-1 antibodies produce a sustained response in some patients with triple-negative breast cancer PD-1 programmed death receptor 1, an important immunosuppressive molecule. PD-1 binding ligands PD-L1 and PD-L2 affect T-cell function, and tumors are able to evade immune surveillance by overexpressing PD-L1, which binds to PD-1. The first early data on the PD-1 immunotherapy Keytruda (pembrolizumab) for metastatic triple-negative breast cancer (TNBC) were presented at the 2014 San Antonio Breast Cancer Conference (SABCS), this time from one of the cohorts of a Phase Ib study (KEYNOTE-012) The cohort investigated Keytruda monotherapy for the treatment of recurrent or TNBC with positive PD-L1 expression. The results showed that Keytruda demonstrated superior antitumor activity against PD-L1 positive triple negative breast cancer, with an overall remission rate of 18.5%, and the investigators of this project intend to conduct a phase II clinical study in the near future. Genotyping to guide treatment is emerging Lehmann et al. first proposed in 2011 that triple negative breast cancer could be classified into six subtypes through genetic analysis – basal-like 1 (BL1), basal-like 2 (BL2), immunomodulatory (IM), mesenchymal-like (M), mesenchymal-like stem (MSL) and tube-like androgen receptor (LAR), and indolent subtype ( UNS). There are some exploratory findings to select the appropriate therapeutic regimens for the characteristics of triple negative breast cancer in different subtypes, such as the BL1 subtype with defective DNA damage repair, which can be preferentially treated with platinum drugs or PARP inhibitors, while the M subtype, BL2 subtype and MSL subtype with multiple signaling pathway activation, select mTOR inhibitors, Src inhibitors, or growth factor inhibitors In a phase II clinical study (TBCRC) reported at the 2014 SABCS meeting, 424 triple negative breast cancers were screened and 28 of them were found to be androgen receptor positive, and 19% of these patients benefited from this treatment after treatment with the androgen antagonist bicalutamide with disease stabilization for more than 6 months. Therefore, androgen receptor antagonist therapy can be administered in triple negative breast cancer. The treatment of metastatic triple-negative breast cancer is difficult, and chemotherapy remains the main treatment modality. Since some patients with triple-negative breast cancer have BRCA1/2 mutations and defective DNA repair, platinum-based chemotherapy regimens can benefit patients with BRCA1/2 mutated triple-negative breast cancer. In addition, bevacizumab could be a treatment option for some triple-negative breast cancers. Other therapeutic agents such as PARP inhibitors, PD-1 antibodies are under clinical investigation and are expected to provide new treatment opportunities for patients with triple negative breast cancer.