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:Quad-Exposed/Refractory Multiple Myeloma: Patients Previously Treated With Anti-CD38, IMiDs, Proteasome Inhibitors, and BCMA-Targeted Therapies.
多发性骨髓瘤的当前治疗方案,无论患者是否适合接受自体干细胞移植且无不良生物学特征(标危细胞遗传学;
目前多发性骨髓瘤的治疗方案,无论患者是否适合自体干细胞移植,只要没有不良生物学特征(标准风险细胞遗传学、无髓外病变、肾功能正常),均可能实现数年至超过10年的无进展生存期。然而,具有不良生物学特征的患者常较早发生疾病进展,最终需要接受多线治疗,以应对逐渐出现的药物耐药。本文聚焦四类药物均耐药的患者,即对蛋白酶体抑制剂、免疫调节药物、抗CD38单克隆抗体和BCMA靶向治疗均耐药者。该人群的治疗选择有限,尤其是既往暴露于抗BCMA治疗或对其耐药,构成治疗疗效的一项重大限制。
Current treatment regimens for multiple myeloma, both in patients eligible and ineligible for autologous stem cell transplantation without adverse biological features (standard risk cytogenetics; absence of extramedullary disease, normal renal function) may achieve progression-free survival lasting from several to over 10 years. However, those patients with adverse biological features, often experience earlier disease progression. Ultimately, these patients require multiple lines of therapy in an attempt to overcome emerging drug resistance. This article focuses on quad-class refractory patients-resistant to proteasome inhibitors, immunomodulatory drugs, anti-CD38 monoclonal antibodies, and BCMA-targeted therapies. Therapeutic options for this patient group are limited, particularly due to anti-BCMA exposure/refractoriness, which represents a major constraint on treatment efficacy.
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