γδ T 细胞调节小细胞肺癌中的抗肿瘤免疫
γδ T cells modulate anti-tumor immunity in small cell lung cancer.
我们的发现表明,活化的γδ T细胞可能是SCLC治疗的有价值靶点。
英文原题:It might be a dead end: immune checkpoint inhibitor therapy in EGFR-mutated NSCLC.
尽管分子靶向治疗取得了创新性进展,但针对表皮生长因子受体(EGFR)突变型非小细胞肺癌(NSCLC)的免疫检查点抑制剂(ICIs)治疗策略尚未取得显著进展。
尽管分子靶向治疗取得了创新性进展,但针对表皮生长因子受体(EGFR)突变非小细胞肺癌(NSCLC)的免疫检查点抑制剂(ICIs)治疗策略并未取得显著进展。越来越多的证据表明,ICI化疗在该人群中效果不足。ICI治疗的生物标志物,如程序性细胞死亡配体1(PD-L1)和TIL(肿瘤浸润淋巴细胞)(TILs),在EGFR突变患者中并非生物标志物,肿瘤微环境的特异性被认为是其原因。PD-L1与细胞毒性T淋巴细胞相关蛋白4(CTLA-4)抑制剂的联合治疗因其严重毒性和有限疗效而令人担忧。然而,早期NSCLC可能与晚期NSCLC不同。在本综述中,我们全面回顾了当前证据,并总结了ICI治疗在EGFR突变患者中的潜力,这些患者在接受EGFR-酪氨酸激酶抑制剂(TKIs)治疗后获得耐药且无T790M突变,或疾病在奥希替尼治疗期间进展。
Despite innovative advances in molecular targeted therapy, treatment strategies using immune checkpoint inhibitors (ICIs) for epidermal growth factor receptor (EGFR)-mutant non-small cell lung cancer (NSCLC) have not progressed significantly. Accumulating evidence suggests that ICI chemotherapy is inadequate in this population. Biomarkers of ICI therapy, such as programmed cell death ligand 1 (PD-L1) and tumor-infiltrating lymphocytes (TILs), are not biomarkers in patients with EGFR mutations, and the specificity of the tumor microenvironment has been suggested as the reason for this. Combination therapy with PD-L1 and cytotoxic T-lymphocyte-associated protein 4 (CTLA-4) inhibitors is a concern because of its severe toxicity and limited efficacy. However, early-stage NSCLC may differ from advanced-stage NSCLC. In this review, we comprehensively review the current evidence and summarize the potential of ICI therapy in patients with EGFR mutations after acquiring resistance to treatment with EGFR-tyrosine kinase inhibitors (TKIs) with no T790M mutation or whose disease has progressed on osimertinib.
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