Triple Negative Breast Cancer: Tumour Biology and Optimisation of Clinical Outcome

Triple negative breast cancer are breast cancer types that are difficult to treat because they lack expression of the estrogen receptor (ER), progesterone receptor (PR) and Human Epidermal Receptor 2 (HER2) gene amplification. Intensive research, analysis by the Cancer Genome Atlas (TCGA) Research Network and the advent of high-throughput technology tools has expanded the classification of TNBC tumors into subgroups according to its gene expression profiles in order to identify the different molecular subtypes, novel TNBC biomarkers that can play both predictive and prognostic roles and enhance therapeutic strategies. The “immune-activated,” subtype or tumours with defective BRCA pathway are amongst initial TNBC group with established genetic vulnerabilities that has allowed the addition of promising therapeutic approaches, including DNA-damaging agents (PARP inhibitors, platinum) as well as immunotherapy. The treatment of metastatic NBC (mTNBC) is currently transforming rapidly with better outcomes observed in clinical trials. The recent success with immune checkpoint inhibitors (ICIs) targeting the programmed cell death receptor 1 and programmed death ligand 1 (PD-L1) and PARP inhibitors for germline BRCA mutation-associated breast cancers as well as other novel strategies in mTNBC treatment will change the course of this unique cancer subtype in the future.