BL1 patients were sensitive to cisplatin treatment. Possible therapeutic drugs for the BL1 subtype include poly (ADP-ribose) polymerase (PARP) inhibitors and genotoxic agents. Gene expression profiling analysis of TNBC tumor samples found abnormal expression of cell cycle-regulating and DNA repair-related genes in the BL1 subtype (high amplification of MYC, PIK3CA, CDK6, AKT2, KRAS, FGFR1, IGF1R, CCNE1, and CDKN2A/B and high frequency of heterozygous or homozygous deletion of DNA repair-related genes such as BRCA2, PTEN, MDM2, RB1, and TP53). This paper reviews existing treatment regimens, therapeutic drugs, and their efficacy in treating TNBC patients and discusses some new preclinical studies and targeted treatment regimens, aiming to provide new ideas and directions for TNBC treatment regimens and targets. Therefore, it is urgent to develop new treatment regimens and targets. Bevacizumab has been used in combination with chemotherapeutic drugs to treat TNBC in some countries, but the survival time of patients did not increase significantly. The residual metastatic lesions eventually will lead to tumor recurrence. Therefore, chemotherapy is the main systemic treatment, but the efficacy of conventional postoperative adjuvant chemoradiotherapy is poor. ĭue to its special molecular phenotype, TNBC is not sensitive to endocrine therapy or molecular targeted therapy. The mortality rate of TNBC patients within 3 months after recurrence is as high as 75%. The average time to relapse in non-TNBC patients is 35–67 months, while that in TNBC patients is only 19–40 months. Distant metastasis mostly occurs in the 3rd year after diagnosis.

The metastasis often involves the brain and visceral organs. The median survival time after metastasis is only 13.3 months, and the recurrence rate after surgery is as high as 25%. TNBC is highly invasive, and approximately 46% of TNBC patients will have distant metastasis. Compared with other subtypes of breast cancer, the survival time of TNBC patients is shorter, and the mortality rate is 40% within the first 5 years after diagnosis. Įpidemiological data show that TNBC mostly occurs in premenopausal young women under 40 years old, who account for approximately 15–20% of all breast cancer patients. The overlap ratio can be as high as 60–90% between TNBC and BLBC, compared to only 11.5% between non-TNBC and BLBC. Approximately 56% of TNBC and BLBC gene expression profiles overlap. Gene expression profiling analysis often classifies TNBC as a subtype of basal-like breast cancer (BLBC). Triple-negative breast cancer (TNBC) is defined as a type of breast cancer with negative expression of estrogen (ER), progesterone (PR), and human epidermal growth factor receptor-2 (HER2). Gallen International Breast Cancer Conference issued a new definition of breast cancer molecular subtypes: luminal A (ER/PR +, HER2 −, Ki67 + < 20%, with the percentage indicating the immunohistochemical staining results for patient samples), luminal B (ER/PR + < 20%, HER2 −, Ki67 + ≥ 20%) HER2 + B2 (ER/PR +, HER2 overexpression), HER2 overexpression (ER −, PR −, HER2 overexpression), basal-like TNBC (ER −, PR −, HER2 −), and other special subtypes.

Clinical treatment and prognosis varies greatly between patients. Breast cancer is a highly heterogeneous disease.

The 2012 global cancer statistics showed that there were approximately 1.7 million women diagnosed with breast cancer, and 521,900 women died of breast cancer. Breast cancer is the most common malignancy in women.

Triple negative breast cancer