决定异体 CAR T 细胞排斥与扩增的细胞和分子机制
Cellular and molecular mechanisms determining allogeneic CAR T cell rejection and expansion.
我们评估了11例接受单一批次cemacabtagene ansegedleucel(cema-cel)治疗的大B细胞淋巴瘤患者,cemacabtagene ansegedleucel是一种异体抗CD19 CAR T产品。
英文原题:CD4+ T-Cell Lymphoma Harboring a Chimeric Antigen Receptor Integration in TP53.
嵌合抗原受体(CAR)T 细胞治疗后的恶性 T 细胞转化已有报道,但 CAR 整合对肿瘤发生的贡献尚不清楚。
嵌合抗原受体(CAR)T 细胞疗法后发生恶性 T 细胞转化的病例已有报道,但 CAR 整合对肿瘤发生的作用尚不明确。我们报告一例 T 细胞淋巴瘤病例,其中慢病毒整合至已知肿瘤抑制基因 TP53;该病例发生于一名多发性骨髓瘤患者接受 B 细胞成熟抗原(BCMA)CAR T 细胞治疗后。
Malignant T-cell transformation after chimeric antigen receptor (CAR) T-cell therapy has been described, but the contribution of CAR integration to oncogenesis is not clear. Here we report a case of a T-cell lymphoma harboring a lentiviral integration in a known tumor suppressor, TP53 , which developed in a patient with multiple myeloma after B-cell maturation antigen (BCMA) CAR T-cell therapy.
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