”Triple negative breast cancer” refers to breast cancer patients who are negative for estrogen receptor (ER), progesterone receptor (PR) and human epidermal growth factor receptor 2 (HER-2). Basal-like breast cancer is characterized by high expression of ER(-)/PR(-)/HER-2(-), which is equivalent to triple-negative breast cancer, and is characterized by high expression of basal High expression of epithelial molecular markers (CK5/6 or 17, EGFR) and low expression of ER or ER-related genes and HER-2 or HER-2-related genes. There is no universally accepted definition of basal cell-like carcinoma, but there are several definitions of basal cell-like carcinoma gene expression as follows: ①ER (-)/HER2 (-), CK5/6 (+) and/or EGFR (+). (ii) CK5/6 (+), caveolin1 (+), CAIX (+), p63 (+) or CD117+. ③CK5/6 (+) and/or CK14 (+). ④CK5/14 (+). The 5-year survival rate of this type of breast cancer is less than 15%, mostly seen in young premenopausal patients, with a higher chance of visceral metastasis and brain metastasis, poor histological grading of pathology, mostly grade 3, a higher proportion of cell proliferation, and mostly with p53 mutation, c-kit, p53, EGFR expression mostly positive, basal cell markers CK5/6, CK17 also mostly positive. The tumor is highly aggressive, prone to local recurrence and distant metastasis, and has more similar features to basal cell-like breast cancer and BRCA1 mutation-associated breast cancer. The prognosis of triple-negative breast cancer has little relationship with tumor size and lymph node status. Recurrence is rapid, with peak recurrence in 1-3 years and peak death in 5 years, with high incidence of brain metastasis and rapid development of distant metastasis leading to death. ”Endocrine therapy and targeted trastuzumab therapy are ineffective in triple negative breast cancer, and chemotherapy is the mainstay of treatment. Compared to other types of breast cancer, triple negative breast cancer is more sensitive to chemotherapy and radiotherapy, but its prognosis is still poor if it is treated with standard conventional therapy, with low recurrence-free survival and overall survival. There are no treatment guidelines for triple-negative breast cancer, and its treatment is generally performed as conventional for poor prognosis breast cancer, with postoperative adjuvant chemotherapy choosing an anthracycline-containing paclitaxel regimen. Neoadjuvant chemotherapy with paclitaxel- and anthracycline-containing regimens is associated with high rates of complete pathological remission. The use of platinum-based agents for neoadjuvant chemotherapy is under investigation. Metastatic triple-negative breast cancer is progressing rapidly and palliative chemotherapy is being investigated with the following: microtubule stabilizers Paclitaxel, Docetaxel, nab-paclitaxel, ixabepilone; carboplatin/cisplatin; anti-angiogenic Bevacizumab, Sunitinib; EGFR inhibitors Cetuximab, Erlotinib, etc. In new drug studies, ezapyrone has been shown to be more effective in combination with capecitabine than capecitabine alone in advanced anthracycline- and paclitaxel-resistant breast cancer and triple-negative breast cancer. Endocrine therapy and trastuzumab-targeted therapy are ineffective in “triple negative breast cancer”, but some triple negative breast cancer patients with high expression of EGFR, c-Kit, CK5/6, P-cadherin, and p53 are expected to benefit from targeted therapy for these patients. The role of cetuximab, a monoclonal antibody to EGFR, and gefitinib and erlotinib, tyrosine kinase inhibitors of EGFR, in the treatment of triple-negative breast cancer is currently being investigated internationally. In many patients with triple-negative breast cancer with BRCA1 deletion or mutation, the risk of developing breast cancer is as high as 82% for those with BRCA1 deletion and 5% for those with BRCA1 mutation due to the important role of BRCA1 in DNA repair mRNA transcription and cell cycle alignment, and related studies have shown that patients with BRCA1 deletion or mutation have a higher risk of developing breast cancer. Patients with BRCA1 deletion or mutation have been shown to be effective with drugs that disrupt the chemical structure of DNA (e.g., alkylating agents, platinum, mitomycin) and less effective with drugs that act on microtubule protein synthesis (e.g., paclitaxel, vincristine). Patients with triple-negative breast cancer did not show a higher rate of local recurrence after breast-conserving surgery and radiotherapy than patients with non-triple-negative breast cancer, i.e., the local recurrence rate of triple-negative breast cancer after radiotherapy was similar to that of non-triple-negative breast cancer. Triple-negative breast cancer is theoretically effective against DNA toxicity drugs and therefore also against radiotherapy.