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
TP53 突变介导的肿瘤免疫逃逸：机制与治疗意义
英文原题：TP53 Mutation-Mediated Immune Evasion in Cancer: Mechanisms and Therapeutic Implications.
查看英文原题
TP53 Mutation-Mediated Immune Evasion in Cancer: Mechanisms and Therapeutic Implications.
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中文摘要
p53突变是癌症发展中最常见的事件，也是由于逃避凋亡级联而导致癌症治疗耐药的主要原因。除了化疗和放疗之外，越来越多的证据表明，p53突变肿瘤对广泛的免疫治疗具有耐药性，如免疫检查点抑制剂、嵌合抗原受体（CAR）T细胞和造血干细胞移植（HSCT）。这凸显了p53突变在驱动肿瘤细胞免疫逃逸中的作用。在这篇综述中，我们首先总结了近期研究，这些研究揭示了p53突变肿瘤逃避T细胞、自然杀伤（NK）细胞和巨噬细胞免疫监视的机制。然后，我们综述了这些突变肿瘤细胞如何重塑肿瘤微环境（TME），调节旁观者细胞如巨噬细胞、中性粒细胞和调节性T（Treg）细胞以促进免疫抑制。此外，我们综述了与p53缺失或突变相关的免疫逃逸的临床观察。最后，我们讨论了增强p53野生型（WT）或突变型肿瘤免疫反应的治疗策略。
展开英文摘要原文
Mutation in p53 is the most frequent event in cancer development and a leading cause of cancer therapy resistance due to evasion of the apoptosis cascade. Beyond chemotherapies and radiation therapies, growing evidence indicates that p53-mutant tumors are resistant to a broad range of immune-based therapies, such as immune checkpoint inhibitors, chimeric antigen receptor (CAR) T, and hematopoietic stem cell transplantation (HSCT).
This highlights the role of p53 mutations in driving immune evasion of tumor cells. In this review, we first summarize recent studies revealing mechanisms by which p53-mutant tumors evade immune surveillance from T cells, natural killer (NK) cells, and macrophages.
We then review how these mutant tumor cells reshape the tumor microenvironment (TME), modulating bystander cells such as macrophages, neutrophils, and regulatory T (Treg) cells to foster immunosuppression.
Additionally, we review clinical observations indicative of immune evasion associated with p53 loss or mutations.
Finally, we discuss therapeutic strategies to enhance immune response in p53 wild-type (WT) or mutant tumors.
论文信息
- 作者
- Wang C、Tan JYM、Chitkara N、Bhatt S
- 单位
- Department of Pharmacy & Pharmaceutical Sciences, National University of Singapore, Singapore 117559, Singapore.Singapore
- 文献类型
- 综述
- 期刊
- Cancers2024 Sep 3
- 原文标识
- PubMed 39272927 · DOI 10.3390/cancers16173069
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