RNF43 p.G659fs 通过 PI3K/AKT/mTOR 信号通路和 HLA-E 上调导致 MSI-high 结直肠癌中 NK 细胞功能障碍
RNF43 p.G659fs leads to natural killer cell dysfunction in MSI-high colorectal cancer through PI3K/AKT/mTOR signaling and HLA-E up-regulation.
CELL INTELLIGENCE · 肿瘤细胞治疗研究
肿瘤细胞治疗研究
英文原题:Immunotherapy resistance in non-small-cell lung cancer: From mechanism to clinical strategies.
Immunotherapy resistance in non-small-cell lung cancer: From mechanism to clinical strategies.
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高原发性耐药发生率和不可避免的继发性耐药是接受免疫治疗的非小细胞肺癌(NSCLC)患者获得持久长期获益的主要临床障碍。NSCLC免疫治疗耐药的机制复杂,主要涉及肿瘤细胞和肿瘤微环境(TME)中浸润的免疫细胞,包括TAMs、B细胞、NK细胞和T细胞。免疫治疗耐药后NSCLC进展的临床策略选择应取决于进展模式。免疫治疗耐药后NSCLC患者的进展模式可分为寡进展和全身性/多发性进展,进一步治疗选择时应考虑这一点。未来需要探索如何优化联合治疗,并探索在肿瘤细胞不同遗传背景下重编程浸润免疫细胞的策略,以及在抗肿瘤治疗过程中及时重塑TME。
The high primary resistance incidence and unavoidable secondary resistance are the major clinical obstacle to lasting long-term benefits in Non-small-cell lung cancer (NSCLC) patients treated with immunotherapy. The mechanisms of immunotherapy resistance in NSCLC are complex, mainly involving tumor cells and tumor microenvironment (TME) infiltrating immune cells, including TAMs, B cells, NK cells, and T cells. The selection of clinical strategies for NSCLC progression after immunotherapy resistance should depend on the progressive mode.
The progression pattern of NSCLC patients after immunotherapy resistance can be divided into oligo-progression and systemic/multiple progression, which should be considered for further treatment selection. In the future, it needs to explore how to optimize the combined therapy and explore strategies to reprogram infiltrating immune cells under various genetic backgrounds of tumor cells and timely reshape TME during antitumor treatments.
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