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Keisuke Kataoka¹, Yuichi Shiraishi², Yohei Takeda³

¹Department of Pathology and Tumor Biology, Graduate School of Medicine, Kyoto University, Kyoto 606-8501, Japan.

|June 10, 2016

概括

破坏PD-L1基因3'区域的结构变异是癌症免疫逃生的一个新机制. 这种PD-L1 3'-UTR干扰提高了PD-L1的表达,帮助瘤逃避并提供了潜在的生物标志物.

科学领域:

癌症学
免疫学
遗传学

背景情况:

针对编程细胞死亡1 (PD-1) 和其配体 (PD- L1) 的抗体已在治疗晚期癌症方面取得成功.
PD-1/PD-L1介导的免疫逃脱在癌症发展中至关重要,但其遗传基础尚未完全理解.
已知的机制包括基因放大和转位驱动的外宫促进剂用于PD-L1升高.

研究的目的:

研究导致PD-L1过度表达和癌症免疫逃逸的新遗传机制.
确定影响PD-L1基因的结构变异及其功能后果.
探索PD- L1 3 - 未翻译区域 (UTR) 干扰作为免疫逃避的生物标志物的潜力.

主要方法:

在各种人类癌症中分析PD-L1基因3区域的结构变异 (SVs).
评估PD-L1转录水平和SV后的稳定性
在体内小鼠模型中评估PD- L1 3 - UTR干扰对瘤免疫逃避和PD- 1/ PD- L1阻塞反应的影响.

主要成果:

在多种癌症中发现常见的破坏PD- L1 3区域的SV,包括成人T细胞白血病/ 淋巴瘤 (27%),扩散大B细胞淋巴瘤 (8%) 和胃腺癌 (2%).
这些SV导致异常PD-L1转录升高,通过3-UTR截断稳定.
在小鼠中,Pd- l1 3 - UTR的干扰促进了瘤的免疫逃避,而瘤对Pd- 1/ Pd- l1阻塞敏感.

结论:

截断PD-L1 3 -UTR的结构变异代表了癌症免疫逃逸的新机制.
这种基因改变导致PD-L1表达的增加,并促进瘤逃避抗瘤免疫力.
PD-L1 3 -UTR的破坏可以作为基因标记来识别使用这种免疫逃避策略的癌症.

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