In recent years, the incidence of TNBC has been increasing, becoming younger, and becoming a hot spot in clinical research. Regardless of the fact that TNBC is generally considered to be highly malignant and has a very poor prognosis, a large number of documents display that TNBC is heterogeneous, showing significant differences in pathological features, biological behaviour and gene expression profiles[8, 9, 10, 11, 12]. Therefore, understanding the TNBC classification has great clinical significance. At present, TNBC has a variety of typing methods and a variety of subtypes with different biological characteristics. By summarising the relevant literature on TNBC classification from 2009 to 2019, Chen Lin  found that the intraluminal androgen receptor (LAR), basal-like (BL), mesenchymal (MES) and immunomodulatory/basal-like immune activation (IM/BLIA) classifications were repeatedly mentioned in several TNBC classifications and are the more accepted ones currently. Joensuu H et al. divided TNBC into BL and non-BL types, of which BL type accounts for 80% and has a high degree of malignancy and poor prognosis compared to non-BL type. Bl-TNBC is divided into BL1 and BL2 types, which are characterized by overexpression of cell cycle-related genes and DNA damage response genes and have a strong proliferative capacity through these features. The top gene ontologies for the BL1 subtype are heavily enriched in cell-cycle and cell division components and pathways (cell-cycle, DNA replication reactome, G2 cell-cycle pathway, RNA polymerase, and G1 to S cell cycle). Elevated DNA damage response (ATR/BRCA) pathways accompany the proliferation pathways in the BL1 subtype. Increased proliferation and cell-cycle checkpoint loss are consistent with the elevated expression of the DNA damage response genes observed. The BL2 type displays a unique gene ontology involving growth factor signalling (EGF pathway, NGF pathway, MET pathway, Wnt/β-catenin and IGF1R pathway), as well as glycolysis and gluconeogenesis. It has features suggestive of a basal/myoepithelial origin and exhibits higher levels of expression of TP63 and MME (CD10).
Recent studies have shown that programmed death ligand 1 (PD-L1) and apurine/pyrimidine endonuclease 1 (APE1) play a role in the development of TNBC, and it is hypothesized that APE1 may be involved in regulating PD-L1 expression, promoting greater metastatic and invasive capacity of tumour cells and further participating in immune escape of tumours  .Accordingly, the emergence of immune checkpoint therapy may be a future research direction. If the process of homologous recombination (HR) is unavailable or impaired, this is referred to as ‘homologous recombination deficiency’ (HRD)[17, 18]. In this situation, DNA repair is more error-prone, which leads to genomic instability. Breast cancer susceptibility genes 1/2 (BRCA1/2) are oncogenes that maintain genomic stability by playing a key role in DNA repair, cell-cycle arrest and transcriptional control. BRCA1 and BRCA2 play a role in the repair of DNA double-strand breaks (DSBs) through the HR process, with BRCA1 guiding the repair towards error-free HR. Loss of BRCA1/2 function leads to HRD , and deletion or mutation of BRCA is closely associated with the development of TNBC. Ki67 significantly correlates with the proliferation level of tumour cells and is predictive of the prognosis of TNBC. Compared to other subtypes of TNBC, BL-1 type has a high value-added rate , indicating active tumour cell proliferation and a poor prognosis.
The diagnosis of breast cancer is made by clinical examination,radiological/imaging examination (including mammography, magnetic resonance imaging (MRI) ultrasonography, etc. and immunohistopathological examination. Early diagnosis of TNBC is difficult and relies on intraoperative rapid frozen section pathological examination and postoperative pathological findings. Surgery combined with neoadjuvant chemotherapy is the main treatment for TNBC. The different histological subtypes of TNBC differ significantly in terms of clinical presentation, treatment and prognosis, and histological classification can help scientists develop the best individualised treatment approach. Platinum drugs and PARP inhibitors  have a helpful effect on BL-1 type of TNBC. Platinum-based drugs affect the replication of double-stranded DNA in tumour cells by cross-linking with their DNA, leading to the death of tumour cells. They are very effective against TNBC caused by impaired repair of genetic damage due to BRCA gene mutations. Mutated BRCA cannot repair DSBs and will result in defects in homologous recombination and cause disease. PARP is a single-strand break (SSB) damage recognition and repair protein that plays an important role in starting SSB repair in DNA through base excision repair. PARP inhibitors can cause accumulation of SSBs, leading to the formation of DSBs for therapeutic purpose.
According to the worldwide classification of intrinsic subtypes, secretory breast carcinoma(SBC) is classified as basal-like TNBC, but the clinical course of SBC is highly indolent. To date, there are no standard treatment guidelines for SBC. It in children is usually solitary, firm, well-defined, less than 20mm in diameter, with good mobility, slow growth, and mostly without lymph node metastasis. In this case, the lesion was simply excised with no tumor cells at the margin, and no incisional enlargement or lymph node dissection was given. Our initial surgical decision was correct in terms of the results of the secondary surgical resection and lymph node dissection. Multiple surgeries caused physical, psychological and financial stress to the child and family to some extent. Our shortcomings were that our anticipatory judgment of the disease and preoperative examination were inadequately prepared, and rapid frozen sections were not performed intraoperatively. At the 1-year postoperative follow-up, the prognosis was good.
SBC belonging to BL-1 type of TNBC has a characteristic t(12:15) equilibrium shift, resulting in the ETV6-NTRK3 gene fusion. Its fusion gene product activates a certain pathway and eventually leads to the production of SBC. The clinical presentation of SBC is mostly benign, and surgical excision is the main option. Depending on the condition, local mass excision or breast-conserving surgical treatment combined with an anterior lymph node biopsy is desirable. However, when local excision is not extensive enough, SBC is at risk of recurrence and metastasis. For SBC patients with infiltration and metastasis, a modified radical mastectomy or radical mastectomy combined with tyrosinase and Ras inhibitor therapy is available.