Mechanism of action and resistance to monoclonal antibody therapy

被引:61
作者
Villamor, N
Montserrat, E
Colomer, D
机构
[1] Hosp Clin Barcelona, Inst Clin Malalties Hematol & Oncol, Unitat Hematopatol, Barcelona 08036, Spain
[2] Hosp Clin Barcelona, Inst Clin Malalties Hematol & Oncol, Hematol Serv, Barcelona 08036, Spain
[3] Inst Invest Biomed August Pi i Sunyer, Barcelona, Spain
关键词
CHRONIC LYMPHOCYTIC-LEUKEMIA; ACUTE MYELOID-LEUKEMIA; NON-HODGKINS-LYMPHOMA; FC-GAMMA-RIIIA; COMPLEMENT-MEDIATED LYSIS; CYTOKINE-RELEASE SYNDROME; RITUXIMAB IN-VITRO; B-CELL LYMPHOMA; TARGETED CHEMOTHERAPY; CAMPATH-1; ANTIGEN;
D O I
10.1016/S0093-7754(03)00261-6
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Monoclonal antibodies (MoAbs) are increasingly used in the treatment of patients with hematological malignancies and autoimmune diseases. The most commonly employed humanized and chimeric MoAbs are rituximab, alemtuzumab (Campath-IH, Ilex Pharmaceuticals, San Antonio, TX), and gemtuzumab-ozogamicin (Mylotarg, Wyeth-Ayerst Laboratories, St Davids, PA). The mechanism of action of these antibodies, and host and cellular factors influencing the response, are not completely known. Induction of apoptosis, antibody-dependent cell cytotoxicity (ADCC), and complement-mediated cell death (CDC) is the proposed mechanism of action of these antibodies. We review the current understanding of the mechanism of action of and resistance to these MoAbs. © 2003 Elsevier Inc. All rights reserved.
引用
收藏
页码:424 / 433
页数:10
相关论文
共 89 条
[1]  
Alas S, 2001, CLIN CANCER RES, V7, P709
[2]   Differential response of human acute myeloid leukemia cells to gemtuzumab ozogamicin in vitro: role of Chk1 and Chk2 phosphorylation and caspase 3 [J].
Amico, D ;
Barbui, AM ;
Erba, E ;
Rambaldi, A ;
Introna, M ;
Golay, J .
BLOOD, 2003, 101 (11) :4589-4597
[3]   Targeted anti-cancer therapy using rituximab, a chimaeric anti-CD20 antibody (IDEC-C2B8) in the treatment of non-Hodgkin's B-cell lymphoma [J].
Anderson, DR ;
GrilloLopez, A ;
Varns, C ;
Chambers, KS ;
Hanna, N .
BIOCHEMICAL SOCIETY TRANSACTIONS, 1997, 25 (02) :705-708
[4]   EXPRESSION OF HUMAN B CELL-ASSOCIATED ANTIGENS ON LEUKEMIAS AND LYMPHOMAS - A MODEL OF HUMAN B-CELL DIFFERENTIATION [J].
ANDERSON, KC ;
BATES, MP ;
SLAUGHENHOUPT, BL ;
PINKUS, GS ;
SCHLOSSMAN, SF ;
NADLER, LM .
BLOOD, 1984, 63 (06) :1424-1433
[5]   The relationship of FcγRIIIa genotype to degree of B cell depletion by rituximab in the treatment of systemic lupus erythematosus [J].
Anolik, JH ;
Campbell, D ;
Felgar, RE ;
Young, F ;
Sanz, I ;
Rosenblatt, J ;
Looney, RJ .
ARTHRITIS AND RHEUMATISM, 2003, 48 (02) :455-459
[6]   Apoptotic-regulatory and complement-protecting protein expression in chronic lymphocytic leukemia: Relationship to in vivo rituximab resistance [J].
Bannerji, R ;
Kitada, S ;
Flinn, IW ;
Pearson, M ;
Young, D ;
Reed, JC ;
Byrd, JC .
JOURNAL OF CLINICAL ONCOLOGY, 2003, 21 (08) :1466-1471
[7]   Complement-mediated cell death induced by rituximab in B-cell lymphoproliferative disorders is mediated in vitro by a caspase-independent mechanism involving the generation of reactive oxygen species [J].
Bellosillo, B ;
Villamor, N ;
López-Guillermo, A ;
Marcé, S ;
Esteve, J ;
Campo, E ;
Colomer, D ;
Montserrat, E .
BLOOD, 2001, 98 (09) :2771-2777
[8]   Phenotypic transformation of CD52pos to CD52neg leukemic T cells as a mechanism for resistance to CAMPATH-1H [J].
Birhiray, RE ;
Shaw, G ;
Guldan, S ;
Rudolf, D ;
Delmastro, D ;
Santabarbara, P ;
Brettman, L .
LEUKEMIA, 2002, 16 (05) :861-864
[9]   Variation in gene expression patterns in follicular lymphoma and the response to rituximab [J].
Bohen, SP ;
Troyanskaya, OG ;
Alter, O ;
Warnke, R ;
Botstein, D ;
Brown, PO ;
Levy, R .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2003, 100 (04) :1926-1930
[10]   Repopulation of blood lymphocyte sub-populations in rheumatoid arthritis patients treated with the depleting humanized monoclonal antibody, CAMPATH-1H [J].
Brett, S ;
Baxter, G ;
Cooper, H ;
Johnston, JM ;
Tite, J ;
Rapson, N .
IMMUNOLOGY, 1996, 88 (01) :13-19