CELL INTELLIGENCE · 肿瘤细胞治疗研究
肿瘤细胞治疗研究
英文原题：CAR+ T-Cell Lymphoma after Cilta-cel Therapy for Relapsed or Refractory Myeloma.
CAR+ T-Cell Lymphoma after Cilta-cel Therapy for Relapsed or Refractory Myeloma.
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我们描述了2例患者，他们在3期CARTITUDE-4试验中接受ciltacabtagene autoleucel（cilta-cel）嵌合抗原受体（CAR）T细胞治疗后发生恶性单克隆T细胞淋巴增殖性疾病。两例患者的单克隆T细胞均可检测到CAR转基因表达和整合。这些CAR转基因T细胞淋巴增殖性肿瘤的临床基因组学特征提示，多种潜在的内在或外在因素（或两者兼有）促成了其发病机制，例如转导了预先存在的TET2突变T细胞，随后获得进一步的致癌基因组变异。其他潜在促成因素包括种系基因组变异、病毒感染以及既往骨髓瘤治疗。在缺乏直接证据的情况下，插入性突变对T细胞淋巴瘤发生的贡献目前尚不清楚。（由Johnson & Johnson和Legend Biotech USA资助；CARTITUDE-4 ClinicalTrials.gov注册号，NCT04181827。）
We describe two patients in whom malignant monoclonal T-cell lymphoproliferation developed after administration of chimeric antigen receptor (CAR) T-cell therapy with ciltacabtagene autoleucel (cilta-cel) in the phase 3 CARTITUDE-4 trial. Monoclonal T cells from both patients had detectable CAR transgene expression and integration. The clinicogenomic features of these CAR transgenic T-cell lymphoproliferative neoplasms suggest that multiple potential intrinsic or extrinsic factors (or both) contributed to their pathogenesis, such as transduction of preexisting TET2 -mutated T cells, followed by acquisition of further oncogenic genomic variants.
Other potential contributors include germline genomic variation, viral infections, and previous treatment for myeloma. In the absence of direct evidence, the contribution of insertional mutagenesis to the development of T-cell lymphoma is currently unclear. (Funded by Johnson & Johnson and Legend Biotech USA; CARTITUDE-4 ClinicalTrials. gov number, NCT04181827.) .
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