ObjectiveTo sort out the key evidence-based data and recent advances in the systemic treatment of advanced triple-negative breast carcinoma (TNBC), to summarize the therapeutic strategies so as to provide guidance for clinical practice. MethodsThe key evidence and research progress on immune checkpoint inhibitors, antibody–drug conjugates (ADCs), poly ADP-ribose polymerase (PARP) inhibitors, anti-angiogenic agents, and novel microtubule inhibitors were summarized. ResultsThe treatment landscape for advanced TNBC has shifted from chemotherapy-centric approaches to biomarker-driven, stratified precision therapy. Based on programmed cell death ligand 1 (PD-L1) expression levels, immune therapy combined with chemotherapy is prioritized. For cases with germline breast cancer gene 1/2 (gBRCA1/2) mutations, PARP inhibitors are recommended. ADCs are suggested for second-line treatment, while novel microtubule inhibitors, either alone or in combination with anti-angiogenic agents, are preferred for later-line therapy to extend patient survival. ConclusionDynamic monitoring of molecular biomarkers such as PD-L1 and gBRCA, combined with sequential or combined "targeted–immunotherapy–ADC" regimens in a "chemotherapy-free" approach, has shown promise in improving overall survival in advanced TNBC.
ObjectiveTo summarize functions and mechanisms of poly ADP-ribose polymerase (PARP) inhibitors and its application in germline BRCA mutated breast cancer.MethodThe literatures about the PARP inhibitors and their applications in the treatment of germline BRCA mutated breast cancer at home and abroad in recent years were collected to make a review.ResultsAs a DNA repair enzyme, the PARP played an important role in the DNA repair pathway. Based on this mechanism, the PARP inhibitors had been developed and widely used in the clinic. On the other hand, the previous studies had shown that the PARP inhibitors marked the synthetic lethal effect in the cancers with homologous recombination deficiency mechanism. By inhibiting the PARP activity in the tumor cells with BRCA mutation, all the DNA damage repair pathways were blocked, which could induce the cell apoptosis or increase the sensitivity of tumor cells to chemoradiotherapy, resulting in the cell death.ConclusionIn patients with germline BRCA mutated breast cancer, PARP inhibitors can selectively kill breast cancer cells and show a high potential for individualized treatment.