雌激素代表的逃学,黄体酮,和人表皮生长因子受体发生在TNBC。与其余乳腺癌(BC)类型相比,TNBC被认为是上复发,诊断较差。目前,因此,TNBC没有批准靶向治疗,治疗方案需要化疗和手术,死亡率很高。因此,本文重点介绍了TNBC的重要通路,并讨论了TNBC治疗的最新进展,包括免疫检查点抑制剂(ICIs),PARP抑制剂,和癌症疫苗。免疫治疗和ICIs,像PD1和PDL1抑制剂,在临床试验(CT)中显示出潜力。这些抑制剂阻碍了允许肿瘤细胞逃避系统的机制,从而增强了人体对TNBC的防御能力。免疫疗法,单独或联合化疗已证明患者的预后,例如生存率提高和治疗相关副作用减少。此外,靶向治疗方法包括BRCA/2突变多聚核糖聚合酶抑制剂,血管内皮生长因子受体(VEGFR)抑制剂,表皮生长因子受体抑制剂,成纤维细胞生长因子抑制剂,雄激素受体抑制剂,PIK3/AKT/mTOR通路抑制剂,细胞周期蛋白依赖性激酶(CDK)抑制剂,Notch信号通路抑制剂,信号转导和转录激活因子3(STAT3)信号通路抑制剂,嵌合抗原受体T(CAR-T)细胞疗法,转化生长因子(TGF)-β抑制剂,表观遗传修饰(EPM)极光激酶抑制剂和抗体-药物缀合物。我们还强调了正在进行的临床试验和TNBC治疗的潜在未来方向。尽管治疗TNBC面临挑战,了解TNBC分子和免疫特性的最新进展为靶向治疗开辟了新的机会,这有望改善这种侵袭性疾病的结果。
The truancy of representation of the estrogen, progesterone, and human epidermal growth factor receptors occurs during TNBC. TNBC is recognized for the upper reappearance and has a poorer diagnosis compared with rest breast cancer (BC) types. Presently, as such, no targeted therapy is approved for TNBC and treatment options are subjected to chemotherapy and surgery, which have high mortality rates. Hence, the current article focuses on the scenario of TNBC vital pathways and discusses the latest advances in TNBC treatment, including immune checkpoint inhibitors (ICIs), PARP suppressors, and cancer vaccines. Immunotherapy and ICIs, like PD 1 and PD L1 suppressors, displayed potential in clinical trials (CTs). These suppressors obstruct the mechanisms which allow tumor cells to evade the system thereby boosting the body\'s defense against TNBC. Immunotherapy, either alone or combined with chemotherapy has demonstrated patient outcomes such as increased survival rates and reduced treatment-related side effects. Additionally, targeted therapy approaches include BRCA/2 mutation poly ribose polymerase inhibitors, Vascular Endothelial Growth Factor Receptor (VEGFR) inhibitors, Epidermal growth factor receptor inhibitors, Fibroblast growth factor inhibitors, Androgen Receptor inhibitors, PIK3/AKT/mTOR pathway inhibitors, Cyclin-dependent kinase (CDK) inhibitors, Notch signaling pathway inhibitors, Signal transducer and activator of transcription 3 (STAT3) signaling pathway inhibitors, Chimeric antigen receptor T (CAR-T) cell therapy, Transforming growth factor (TGF) -β inhibitors, Epigenetic modifications (EPM), Aurora Kinase inhibitors and antibody-drug conjugates. We also highlight ongoing clinical trials and potential future directions for TNBC therapy. Despite the challenges in treating TNBC, recent developments in understanding the molecular and immune characteristics of TNBC have opened up new opportunities for targeted therapies, which hold promise for improving outcomes in this aggressive disease.