FcγRIIIa and FcγRIIa polymorphisms do not predict response to rituximab in B-cell chronic lymphocytic leukemia

Blood

Volumn 103, Issue 4, 2004, Pages 1472-1474

  Farag, Sherif S ^b   Flinn, Ian W ^b   Modali, Rama ^b   Lehman, Teresa A ^b   Young, Donn ^b   Byrd, John C ^a  

^a OHIO STATE UNIVERSITY   (United States)

^b NONE

Author keywords

[No Author keywords available]

Indexed keywords

FC GAMMA RECEPTOR 2A; FC GAMMA RECEPTOR 3A; FC RECEPTOR; RITUXIMAB; UNCLASSIFIED DRUG;

ADULT; AGED; ANTIBODY DEPENDENT CELLULAR CYTOTOXICITY; ARTICLE; B LYMPHOCYTE; CANCER PATIENT; CHRONIC LYMPHATIC LEUKEMIA; CLINICAL ARTICLE; CONTROLLED STUDY; CORRELATION ANALYSIS; DRUG INFUSION; DYSPNEA; FEMALE; GENETIC POLYMORPHISM; HUMAN; HUMAN CELL; HYPOTENSION; HYPOXIA; MALE; PHENOTYPE; PREDICTION; PRIORITY JOURNAL; SIDE EFFECT; TREATMENT OUTCOME;

EID: 0842264005     PISSN: 00064971     EISSN: None     Source Type: Journal    
DOI: 10.1182/blood-2003-07-2548     Document Type: Article

References (24)

1. Maloney DG, Grillo-Lopez AJ, Bodkin DJ, et al. IDEC-C2B8: results of a phase I multiple-dose trial in patients with relapsed non-Hodgkin's lymphoma. J Clin Oncol. 1997;15:3266-3274.
2. McLaughlin P, Grillo-Lopez AJ, Link BK, et al. Rituximab chimeric anti-CD20 monoclonal antibody therapy for relapsed indolent lymphoma: half of patients respond to a four-dose treatment program. J Clin Oncol. 1998;16:2825-2833.
3. O'Brien SM, Kantarjian H, Thomas DA, et al. Rituximab dose-escalation trial in chronic lymphocytic leukemia. J Clin Oncol. 2001;19:2165-2170.
4. Byrd JC, Murphy T, Howard RS, et al. Rituximab using a thrice weekly dosing schedule in B-cell chronic lymphocytic leukemia and small lymphocytic lymphoma demonstrates clinical activity and acceptable toxicity. J Clin Oncol. 2001;19:2153-2164.
5. Reff M, Carner K, Chambers KS, et al. Depletion of B cells in vivo by a chimeric mouse human monoclonal antibody to CD20. Blood. 1994;83:435-445.
6. Golay J, Zaffaroni L, Vaccari T, et al. Biologic response of B lymphoma cells to anti-CD20 monoclonal antibody rituximab in vitro: CD55 and CD59 regulate complement-mediated cell lysis. Blood. 2000;95:3900-3908.
7. Harjunpaa A, Junnikkala S, Meri S, et al. Rituximab (anti-CD20) therapy of B-cell lymphomas: direct complement killing is superior to cellular effector mechanisms. Scand J Immunol. 2000;51:634-641.
8. Maloney D, Smith B. The anti-tumor effect of monoclonal anti-CD20 antibody (MAB) therapy includes direct anti-proliferative activity and induction of apoptosis in CD20 positive non-Hodgkin's lymphoma (NHL) cell lines [abstract]. Blood. 1996;88:637.
9. Hofmeister JK, Cooney D, Coggeshall KM. Clustered CD20 induced apoptosis: src-family kinase, the proximal regulator of tyrosine phosphorylation, calcium influx, and caspase 3-dependent apoptosis. Blood Cells Mol Dis. 2000;26:133-143.
10. Ghetie MA, Bright H, Vitetta ES. Homodimers but not monomers of Rituxin (chimeric anti-CD20) induce apoptosis in human B-lymphoma cells and synergize with a chemotherapeutic agent and an immunotoxin. Blood. 2001;97:1392-1398.
11. Clynes RA, Towers TL, Presta LG, et al. Inhibitory Fc receptors modulate in vivo cytotoxicity against tumor targets. Nat Med. 2000;6:443-446.
12. Cartron G, Dacheux L, Salles G, et al. Therapeutic activity of humanized anti-CD20 monoclonal antibody and polymorphism in IgG Fc receptor FcγRIIIa gene. Blood. 2002;99:754-758.
13. Wu J, Edberg JC, Radecha PB, et al. A novel polymorphism of FcγRIIIa (CD16) alters receptor function and predisposes to autoimmune disease. J Clin Invest. 1997;100:1059-1070.
14. Koene HR, Kleijer M, Algra J, et al. FcγRIIIa-158V/F polymorphism influences the binding of IgG by natural killer cell FcγRIIIa, independently of the FcγRIIIa-48L/R/H phenotype. Blood. 1997;90:1109-1114.
15. Binstadt BA, Geha RS, Bonilla F. IgG Fc receptor polymorphisms in human disease: implications for intravenous immunglobulin therapy. J Allergy Clin Immunol. 2003;111:697-703.
16. Kay NE, Hamblin TJ, Jelinek DF, et al. Chronic lymphocytic leukemia. Hematology (Am Soc Hematol Educ Program). 2002:193-213.
17. Rosenwald A, Alizadeh AA, Widhopf G, et al. Relation of gene expression phenotype to immunoglobulin mutation genotype in B cell chronic lymphocytic leukemia. J Exp Med. 2001;194:1639-1647.
18. Bellosillo B, Villamor N, Lopez-Guillermo A, et al. 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. Blood. 2001;98:2771-2777.
19. Byrd JC, Kitada S, Flinn IW, et al. The mechanism of tumor cell clearance by rituximab in vivo in patients with B-cell chronic lymphocytic leukemia: evidence of caspase activation and apoptosis induction. Blood. 2002;99:1038-1043.
20. Cheson BD, Bennett JM, Grever M, et al. National Cancer Institute-sponsored Working Group guidelines for chronic lymphocytic leukemia: revised guidelines for diagnosis and treatment. Blood. 1996;87:4990-4997.
21. Harris NL, Jaffe ES, Diebold J, et al. World Health Organization classification of neoplastic diseases of the hematopoietic and lymphoid tissues: report of the Clinical Advisory Committee meeting-Airlie House, Virginia, November 1997. J Clin Oncol. 1999;17:3835-3849.
22. Ansell SM, Witzig TE, Kurtin PJ, et al. Phase 1 study of interleukin-12 in combination with rituximab in patients with B-cell non-Hodgkin lymphoma. Blood. 2002;99:67-74.
23. Bannerji R, Kitada S, Flinn IW, et al. Apoptotic-regulatory and complement-protecting protein expression in chronic lymphocytic leukemia: relationship to in vivo rituximab resistance. J Clin Oncol. 2003;21:1466-1471.
24. Byrd J, Smith L, Hackbarth M, et al. Interphase cytogenetic abnormalities in chronic lymphocytic leukemia predict response to rituximab. Cancer Res. 2003;63:36-38.