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 and immunoevasion of colorectal cancer.
Immunotherapy and immunoevasion of colorectal cancer.
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免疫治疗在临床试验中取得的巨大成功,已使其成为癌症治疗的新支柱。然而,在构成大多数CRC肿瘤的微卫星稳定结直肠癌(MSS-CRC)中,临床疗效甚微。在此,我们讨论CRC的分子和遗传异质性。我们回顾免疫逃逸机制,并重点关注免疫治疗作为CRC治疗手段的最新进展。通过更好地理解肿瘤微环境(TME)和免疫逃逸的分子机制,本综述为开发对不同CRC亚群患者有效的治疗策略提供了见解。
The tremendous success of immunotherapy in clinical trials has led to its establishment as a new pillar of cancer therapy.
However, little clinical efficacy has been achieved in microsatellite stable colorectal cancer (MSS-CRC), which constitutes most CRC tumors.
Here, we discuss the molecular and genetic heterogeneity of CRC.
We review the immune escape mechanisms, and focus on the latest advances in immunotherapy as a treatment modality for CRC. By providing a better understanding of the tumor microenvironment (TME) and the molecular mechanisms underlying immunoevasion, this review offers an insight into developing therapeutic strategies that are effective for patients with various subsets of CRC.
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