Glucocorticoids and rituximab in vitro: Synergistic direct antiproliferative and apoptotic effects

Blood

Volumn 100, Issue 5, 2002, Pages 1765-1773

  Rose, Andrea L ^a,b   Smith, Barbara E ^a   Maloney, David G ^a  

^a Fred Hutchinson Cancer Research Center   (United States)

^b NONE   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

DEXAMETHASONE; DNA; GLUCOCORTICOID; PHOSPHATIDYLSERINE; RITUXIMAB;

ANTIBODY DEPENDENT CELLULAR CYTOTOXICITY; APOPTOSIS; ARTICLE; CANCER CELL CULTURE; CANCER INHIBITION; CELL CYCLE G1 PHASE; CELL MEDIATED CYTOTOXICITY; CELL PROLIFERATION; COMPLEMENT DEPENDENT CYTOTOXICITY; CYTOLYSIS; CYTOTOXICITY; DNA CONTENT; DRUG POTENTIATION; HUMAN; HUMAN CELL; NONHODGKIN LYMPHOMA; PREMEDICATION; PRIORITY JOURNAL;

EID: 0036721023     PISSN: 00064971     EISSN: None     Source Type: Journal    
DOI: 10.1182/blood.v100.5.1765.h81702001765_1765_1773     Document Type: Article

References (39)

1. Depletion of B cells in vivo by a chimeric mouse human monoclonal antibody to CD20
2. Signaling events involved in anti-CD20-induced apoptosis of malignant human B cells
3. Clustered CD20 induced apoptosis: src-family kinase, the proximal regulator of tyrosine phosphorylation, calcium influx, and caspase 3-dependent apoptosis
4. Homodimers but not monomers of Rituxan (chimeric anti-CD20) induce apoptosis in human B-lymphoma cells and synergize with a chemotherapeutic agent and an immunotoxin
5. Apoptosis of malignant human B cells by ligation of CD20 with monoclonal antibodies
6. Identification of a cytoplasmic region of CD20 required for its redistribution to a detergent-insoluble membrane compartment
7. Glucocorticoid-induced apoptosis of human leukemic cells is caused by the repressive function of the glucocorticoid receptor
8. Glucocorticoid hormones inhibit DNA synthesis and enhance Interferon production in human lymphoid cell line
9. Dexamethasone induces irreversible G1 arrest and death of a human lymphoid cell line
10. Glucocorticoid-induced thymocyte apoptosis is associated with endogenous endonuclease activation
11. Involvement of BCL-2 in glucocorticoid-induced apoptosis of human pre-B-leukemias
12. Bcl-2 inhibits glucocorticoid-induced apoptosis but only partially blocks calcium lonophore or cycloheximideregulated apoptosis in S49 cells
13. Characterization of the in vitro effects of glucocorticosteroids on NK cell activity
14. Inhibition by cortisol of human natural killer (NK) cell activity
15. Potential role for concurrent abnormalities of the cyclin D1, p16CDKN2 and p16CDKN2B genes in certain B cell non-Hodgkin's lymphomas: Functional studies in a cell line (Granta 519)
16. Characterization of a new non-Hodgkin's lymphoma cell line (NCEB-1) with a chromosomal (11:14) translocation [t(11:14)(q13;q32)]
17. Apoptosis induction by the glucocorticoid hormone dexamethasone and the calclum-ATPase inhibitor thapsigargin involves Bc1-2 regulated caspase activation
18. Inhibition of interleukin 10 by rituximab results in down-regulation of bcl-2 and sensitization of B-cell non-hodgkin's lymphoma to apoptosis
19. + concentration
20. Dexamethasone induces apoptosis of multiple myeloma cells in a JNK/SAP kinase independent mechanism
21. Glucocorticoid activation of a calcium-dependent endonuclease in thymocyte nuclei leads to cell death
22. Calcium dependence of glucocorticoid-induced lymphocytolysis
23. c-Myc and cyclin D3 (CcnD3) genes are independent targets for glucocorticoid inhibition of lymphoid cell proliferation
24. Glucocorticoid regulation of transcription of the c-myc cellular protooncogene in P1798 cells
25. Glucocorticoid inhibition of c-myc, c-myb, and c-Ki-ras expression in a mouse lymphoma cell line
26. Glucocorticoid regulation of cyclin D3 gene transcription and mRNA stability in lymphoid cells
27. Glucocorticoid antagonist RU 486 reverses agonist-induced apoptosis and c-myc repression in human leukemic CEM-C7 cells
28. Suppression of c-myc is a critical step in glucocorticoid-induced human leukemic cell lysis
29. Biologic response of B lymphoma cells to anti-CD20 monoclonal antibody rituximab in vitro: CD55 and CD59 regulate complement-mediated cell lysis
30. Targeted anti-cancer therapy using rituximab, a chimaeric anti-CD20 antibody (IDEC-C2B8) in the treatment of non-Hodgkin's B-cell lymphoma
31. Rituximab (anti-CD20) therapy of B-cell lymphomas: Direct complement killing is superior to cellular effector mechanisms
32. 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
33. CD20 levels determine the in vitro susceptibility to rituximab and complement of B-cell chronic lymphocytic leukemia: Further regulation by CD55 and CD59
34. Tumor cell expression of CD59 is associated with resistance to CD20 serotherapy in patients with B-cell malignancies
35. Expression of complement inhibitors CD46, CD55, and CD59 on tumor cells does not predict clinical outcome after rituximab treatment in follicular non-Hodgkin lymphoma
36. Effector cell-mediated mechanisms play the dominant role in the cytotoxicity of Rituximab on human peripheral blood B cells from normal donors and patients with chronic lymphocytic leukemia
37. Inhibitory Fc receptors modulate in vivo cytoxicity against tumor targets
38. Fc-γRIIIa-158V/F polymorphism influences the binding of IgG by natural killer cell Fc γRIII, independently of the FcγRIIIa-48L/R/H phenotype
39. Therapeutic activity of humanized anti-CD20 monoclonal antibody and polymorphism in IgG Fc receptor FcγRIIIa gene