美罗华
切碎
单克隆抗体
滤泡性淋巴瘤
补体依赖性细胞毒性
淋巴瘤
细胞毒性
抗体
长春新碱
CD20
医学
癌症研究
环磷酰胺
抗体依赖性细胞介导的细胞毒性
化疗
免疫学
体外
生物
内科学
生物化学
作者
Thomas Cerny,Bettina Borisch,Martino Introna,Peter Johnson,Andrea L. Rose
出处
期刊:Anti-Cancer Drugs
[Ovid Technologies (Wolters Kluwer)]
日期:2002-11-01
卷期号:13: S3-S10
被引量:216
标识
DOI:10.1097/00001813-200211002-00002
摘要
Rituximab, the humanized chimeric anti-CD20 monoclonal antibody, represents a powerful tool for treating B-cell malignancies and is licensed for the treatment of relapsed or chemorefractory low-grade or follicular non-Hodgkin's lymphoma (NHL). It has a unique mode of action and can induce killing of CD20+ cells via multiple mechanisms. The direct effects of rituximab include complement-mediated cytotoxicity and antibody-dependent cellmediated cytotoxicity, and the indirect effects include structural changes, apoptosis, and sensitization of cancer cells to chemotherapy.In vitrostudies have made a significant contribution to the understanding of these mechanisms of action and have led to the development of innovative and effective treatment strategies to optimize patient response. The most significant of these strategies is the combination of rituximab and CHOP chemotherapy (cyclophosphamide, doxorubicin, vincristine and prednisone), which is proving a highly effective combination in the treatment of NHL. However, all patients do not respond equally well to rituximab, andin vitrostudies have identified a possible mechanism of resistance involving the anti-complement inhibitors CD55 and CD59. Neutralizing antibodies to CD55 and CD59 can overcome resistance to rituximab-mediated complement-mediated cytotoxicityin vitro.This paper overviews our understanding of the mechanisms of action of rituximab and identifies how this knowledge could be applied in a clinical setting to maximize response in both sensitive and resistant patients.
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