肿瘤细胞治疗研究
英文原题：Recent Advances in Immunotherapy and Targeted Therapy of Triple Negative Breast Cancer.
在TNBC期间，雌激素、孕激素和人表皮生长因子受体的代表性缺失。
在TNBC中，雌激素、孕激素和人表皮生长因子受体的代表性缺失。TNBC以其高复发率和相比其他乳腺癌（BC）类型更差的诊断而闻名。目前，针对TNBC尚无靶向治疗获批，治疗选择仅限于化疗和手术，这些方法具有较高的死亡率。因此，本文聚焦于TNBC关键通路的现状，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，如PD 1和PD L1抑制剂，在临床试验（CTs）中显示出潜力。这些抑制剂阻断了允许肿瘤细胞逃避免疫系统的机制，从而增强了机体对TNBC的防御。免疫治疗，无论是单独使用还是与化疗联合，均已显示出患者结局的改善，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、CAR-T（CAR-T）细胞疗法、转化生长因子（TGF）抑制剂、表观遗传修饰（EPM）、Aurora激酶抑制剂和抗体-药物偶联物。我们还重点介绍了正在进行的临床试验以及TNBC治疗的潜在未来方向。尽管治疗TNBC面临挑战，但近期对TNBC分子和免疫特征认识的进展为靶向治疗开辟了新机遇，有望改善这种侵袭性疾病的预后。
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) - 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.
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