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实体瘤中放疗增强 B7-H3 靶向 CAR T 细胞活性

英文原题:B7-H3-targeted CAR T cell activity is enhanced by radiotherapy in solid cancers.

PubMed 2023/07/07(内容时间) Front Oncol Q2 · IF 3.4(JCR 2025)

研究概要

利用经基因修饰以表达嵌合抗原受体(CAR)的T细胞进行的过继性细胞疗法,已在血液系统恶性肿瘤中展现出有前景的临床结果。

中文摘要

利用基因修饰表达嵌合抗原受体(CAR)的T细胞进行的过继细胞疗法已在血液系统恶性肿瘤中显示出有前景的临床结果。然而,由于多重障碍,实体瘤尚未取得类似的成功。研究这些逃逸机制并设计应对此类局限性的策略至关重要且恰逢其时。文献中越来越多的证据支持以下假设:放疗有潜力通过克服耐药机制来增强实体瘤对CAR T细胞疗法的易感性。放射治疗可以增加不同类型实体瘤(TNBC、HNSCC、PDAC)对B7-H3 CAR T细胞介导的清除的易感性。多种机制,包括减少癌细胞增殖、上调靶抗原、调节凋亡分子,可能促成了这一信号。文献中的信息以及我们所描述的结果支持放疗能够提高CAR T细胞疗法在实体瘤中的疗效。

展开英文摘要原文

Adoptive cell therapy utilizing T cells genetically modified to express a chimeric antigen receptor (CAR) has demonstrated promising clinical results in hematological malignancies. However, solid cancers have not seen a similar success due to multiple obstacles. Investigating these escape mechanisms and designing strategies to counteract such limitations is crucial and timely. Growing evidence in the literature supports the hypothesis that radiotherapy has the potential to enhance the susceptibility of solid tumors to CAR T cell therapy, by overcoming mechanisms of resistance. Radiation treatment can increase the susceptibility of different types of solid cancers (TNBC, HNSCC, PDAC) to B7-H3 CAR T cell-mediated eradication. Multiple mechanisms, including reduced cancer cell proliferation, upregulation of the targeted antigen, modulation of apoptotic molecules may contribute to this signal. The information in the literature and the results we describesupport the ability of radiotherapy to improve the efficacy of CAR T cell therapy in solid tumors.

论文信息

作者
Ventin M、Cattaneo G、Maggs L、Jia J、Arya S、Ferrone S、Wang X、Ferrone CR
第一作者单位
Division of Gastrointestinal and Oncologic Surgery, Department of Surgery, Massachusetts General Hospital, Harvard Medical School, Boston, MA, United States.United States
通讯作者单位
Department of Surgery, Cedars Sinai Medical Center, Los Angeles, CA, United States.United States
期刊
Frontiers in oncology2023
原文标识
PubMed 37483496 · DOI 10.3389/fonc.2023.1193963