Zarychta Julia, Kowalczyk Adrian, Marszołek Anna, Zawitkowska Joanna, Lejman Monika
Student Scientific Society of Department of Pediatric Hematology, Oncology and Transplantology, Medical University of Lublin, Lublin, Poland.
Student Scientific Society of Independent Laboratory of Genetic Diagnostics, Medical University of Lublin, Lublin, Poland.
Ther Adv Med Oncol. 2024 Aug 15;16:17588359241266140. doi: 10.1177/17588359241266140. eCollection 2024.
Despite significant progress in the treatment of some types of cancer, high-grade gliomas (HGGs) remain a significant clinical problem. In the case of glioblastoma (GBM), the most common solid tumor of the central nervous system in adults, the average survival time from diagnosis is only 15-18 months, despite the use of intensive multimodal therapy. Chimeric antigen receptor (CAR)-expressing T cells, which have already been approved by the Food and Drug Administration for use in the treatment of certain hematologic malignancies, are a new, promising therapeutic option. However, the efficacy of CAR-T cells in solid tumors is lower due to the immunosuppressive tumor microenvironment (TME). Reprogramming the immunosuppressive TME toward a pro-inflammatory phenotype therefore seems particularly important because it may allow for increasing the effectiveness of CAR-T cells in the therapy of solid tumors. The following literature review aims to present the results of preclinical studies showing the possibilities of improving the efficacy of CAR-T in the TME of GBM by reprogramming the TME toward a pro-inflammatory phenotype. It may be achievable thanks to the use of CAR-T in a synergistic therapy in combination with oncolytic viruses, radiotherapy, or epigenetic inhibitors, as well as by supporting CAR-T cells crossing of the blood-brain barrier, normalizing impaired angiogenesis in the TME, improving CAR-T effector functions by cytokine signaling or by blocking/knocking out T-cell inhibitors, and modulating the microRNA expression. The use of CAR-T cells modified in this way in synergistic therapy could lead to the longer survival of patients with HGG by inducing an endogenous anti-tumor response.
尽管在某些类型癌症的治疗方面取得了重大进展,但高级别胶质瘤(HGGs)仍然是一个严重的临床问题。就胶质母细胞瘤(GBM)而言,它是成人中枢神经系统最常见的实体瘤,尽管采用了强化多模式治疗,但从诊断起的平均生存时间仅为15 - 18个月。嵌合抗原受体(CAR)表达T细胞已被美国食品药品监督管理局批准用于治疗某些血液系统恶性肿瘤,是一种新的、有前景的治疗选择。然而,由于免疫抑制性肿瘤微环境(TME),CAR - T细胞在实体瘤中的疗效较低。因此,将免疫抑制性TME重编程为促炎表型显得尤为重要,因为这可能会提高CAR - T细胞在实体瘤治疗中的有效性。以下文献综述旨在展示临床前研究结果,这些结果表明通过将TME重编程为促炎表型来提高CAR - T在GBM的TME中的疗效的可能性。这可能通过在协同治疗中联合使用CAR - T与溶瘤病毒、放射疗法或表观遗传抑制剂来实现,还可通过支持CAR - T细胞穿越血脑屏障、使TME中受损的血管生成正常化、通过细胞因子信号传导或通过阻断/敲除T细胞抑制剂来改善CAR - T效应功能以及调节微小RNA表达来实现。在协同治疗中使用以这种方式修饰的CAR - T细胞可能通过诱导内源性抗肿瘤反应来延长HGG患者的生存期。