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:From Multiple Myeloma to Acute Myeloid Leukemia: A Case Report of a 61-year-old Woman after 8 Years of Chemotherapy and Immunotherapy.
在本病程中,疾病复发了两次,其中一次表现为轻链逃逸(LCE)。此外,通过该患者的疾病过程,我们回顾了可能相关的克隆演变过程。
作为第二常见的血液系统恶性肿瘤,多发性骨髓瘤(MM)影响浆细胞,其特征是染色体异常,特别是涉及免疫球蛋白重链转换区。MM代表一种生物学和临床上异质性的血液系统恶性肿瘤,可作为克隆演变的模型,从意义未明的单克隆丙种球蛋白病(MGUS)和冒烟型多发性骨髓瘤(SMM)到MM的所有阶段均表现出克隆异质性。尽管MM的治疗已取得重大进展,患者预后得到改善,但由于预先存在的耐药克隆的存在和选择或治疗期间的选择压力,疾病复发的问题日益引起关注。病例介绍:我们报告一例女性多发性骨髓瘤(MM)患者,她接受了8年的治疗过程,包括化疗、免疫调节剂、造血干细胞移植、CD38单克隆抗体和CAR-T 细胞,最近被诊断为同时患有进展性MM和急性髓系白血病(AML)。该患者见证了MM治疗模式的演变。
BACKGROUND: As the second most prevalent hematologic malignancy, multiple myeloma (MM) affects plasma cells and is characterized by chromosomal abnormalities, particularly involving the immunoglobulin heavy chain switch region. MM represents a biologically and clinically heterogeneous hematological malignancy that serves as a clonal evolution model, exhibiting clonal heterogeneity throughout all stages from monoclonal gammopathy undetermined significance (MGUS) and smoldering multiple myeloma (SMM) to MM. Although significant progress has been made in the treatment of MM, leading to improved patient outcomes, concerns are arising regarding disease relapse due to the presence and selection of pre-existing resistant clones or selective pressure during therapy. CASE PRESENTATION: We present a case of multiple myeloma (MM) in a female patient, who underwent an 8-year course of treatment, including chemotherapy, immunomodulators, hematopoietic stem cell transplantation, CD38 monoclonal antibody, and chimeric antigen receptor T-cell (CAR-T), and was recently diagnosed with concurrent progressive MM and acute myeloid leukemia (AML). This patient has witnessed the evolution of MM treatment paradigms. CONCLUSION: In this course, disease relapses occurred twice, one of which was manifested by a light chain escape (LCE). Moreover, through the course of the disease in this patient, we review the process of clonal evolution that may be relevant.
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