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抑制EZH1/EZH2增强了针对多种癌症模型的采用性T细胞免疫疗法

Patrizia Porazzi¹, Siena Nason¹, Ziqi Yang¹

¹Center for Cellular Immunotherapies, University of Pennsylvania, Philadelphia, PA, USA; Division of Hematology-Oncology, Hospital of the University of Pennsylvania, Philadelphia, PA, USA; Lymphoma Program, Abramson Cancer Center, University of Pennsylvania, Philadelphia, PA, USA.

|February 21, 2025

概括

抑制EZH1/2甲基转移酶可以重编程瘤,使其更具免疫性,从而提高了仿真抗原受体T细胞 (CAR-T) 治疗的疗效. 这种方法在各种癌症的临床前模型中增强了采用细胞免疫疗法.

科学领域:

免疫学免疫学免疫学
在瘤学瘤学.
表观遗传学在表观遗传学中,表观遗传学是指表观遗传学.

背景情况:

瘤对仿真抗原受体T细胞 (CAR-T) 和采用细胞免疫疗法 (ACT) 的耐药性是一个重要的临床障碍.
表观遗传修饰,特别是甲基转移酶活性,在癌症免疫逃避中发挥作用.

研究的目的:

研究是否抑制EZH2和EZH1甲基转移酶可以提高CAR-T细胞治疗的疗效.
确定EZH1/2抑制是否会将瘤重新编程到更具免疫性的状态,从而改善ACT的结果.

主要方法:

在临床前癌症模型中使用EZH2抑制剂 (tazemetostat) 和联合EZH1/EZH2抑制剂 (valemetostat).
评估了CAR-T细胞激活,扩张,瘤透以及在各种液体和固体癌症中的整体疗效.
分析了与免疫反应和瘤细胞激发相关的基因表达变化.

主要成果:

使用tazemetostat抑制EZH2,通过增强T细胞功能和瘤透,提高了B细胞淋巴瘤中抗CD19CAR-T疗效.
塔泽梅托斯塔特治疗导致粘附的上调,B细胞激活和炎症反应基因,增加了CAR-T热情.
联合EZH1/EZH2抑制与valemetostat进一步提高了CAR-T的疗效和扩散在多种癌症类型.

结论:

抑制EZH1/2有效地将瘤重新编程成一种更具免疫性的表型.
针对EZH1/2是一个有前途的策略,可以克服耐药性并提高CAR-T和其他ACT在各种癌症中的有效性.

关键词:

这是一种B细胞淋巴瘤.在CART-T中,我们可以使用CAR-T.在 EZH1 中.在 EZH2 中使用.T细胞受体受体的 T 细胞受体.收养的T细胞疗法仿制性抗原受体T细胞的T细胞.表观遗传学是指表观遗传学.多发性骨髓瘤是多发性骨髓瘤的一种疾病.固体癌症是一种固体癌症.塔泽姆天气统计局值得一提的是气象状况.

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