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:NCCN Guidelines® Insights: Chronic Lymphocytic Leukemia/Small Lymphocytic Lymphoma, Version 2.2026.
Bruton酪氨酸激酶抑制剂(BTKis)和含BCL2抑制剂(BCL2i)的方案显著改善慢性淋巴细胞白血病/小淋巴细胞淋巴瘤(CLL/SLL)患者的生存结局。
Bruton酪氨酸激酶抑制剂(BTKis)和含BCL2抑制剂(BCL2i)的方案显著改善慢性淋巴细胞白血病/小淋巴细胞淋巴瘤(CLL/SLL)患者的生存结局。随机临床试验结果表明,与BTKi单药治疗或化学免疫治疗(CIT)相比,含BCL2i方案的限时治疗可获得更高的不可检测可测量残留病(uMRD)率。Pirtobrutinib(一种非共价BTKi)和lisocabtagene maraleucel(CD19靶向CAR T细胞疗法)是既往接受BTKi和含BCL2i方案治疗后复发或难治性疾病的新选择。CLL/SLL向弥漫性大B细胞淋巴瘤的组织学转化(Richter转化)与不良预后相关。通过分子分析确定CLL/SLL与转化性弥漫性大B细胞淋巴瘤之间是否存在克隆关系,有助于选择合适的治疗方案。本NCCN指南见解重点介绍了NCCN指南中关于CLL/SLL和Richter转化治疗的重大更新。
Bruton tyrosine kinase inhibitors (BTKis) and BCL2 inhibitor (BCL2i)-containing regimens significantly improve survival outcomes in patients with chronic lymphocytic leukemia/small lymphocytic lymphoma (CLL/SLL). Results from randomized clinical trials have demonstrated that time-limited treatment with BCL2i-containing regimens resulted in higher rates of undetectable measurable residual disease (uMRD) than BTKi monotherapy or chemoimmunotherapy (CIT). Pirtobrutinib (a noncovalent BTKi) and lisocabtagene maraleucel (CD19-directed CAR T-cell therapy) are newer options for relapsed or refractory disease after prior therapy with BTKi and BCL2i-contining regimens. Histologic transformation of CLL/SLL to diffuse large B-cell lymphoma (Richter transformation) is associated with a poor prognosis. Molecular analysis to determine whether there is clonal relationship between CLL/SLL and transformed diffuse large B-cell lymphoma is useful to select an appropriate treatment option. These NCCN Guideline Insights highlight significant updates to the NCCN Guidelines for the treatment of CLL/SLL and Richter transformation.
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