Addition of rituximab to standard chemotherapy improves the survival of both the germinal center B-cell-like and non-germinal center B-cell-like subtypes of diffuse large B-cell lymphoma.
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W. Chan | T. Greiner | D. Weisenburger | J. Armitage | K. Fu | W. Choi | K. Perry | Lynette M. Smith | X. Shi | C. Hans | P. Bierman | R. Bociek | J. Vose | Xinlan Shi | Kyle D. Perry
[1] P. Chinn,et al. Depletion of B cells in vivo by a chimeric mouse human monoclonal antibody to CD20. , 1994, Blood.
[2] M. Piris,et al. p53 and bcl-2 expression in high-grade B-cell lymphomas: correlation with survival time. , 1994, British Journal of Cancer.
[3] D C Linch,et al. Prognostic significance of BCL-2 expression and bcl-2 major breakpoint region rearrangement in diffuse large cell non-Hodgkin's lymphoma: a British National Lymphoma Investigation Study. , 1996, Blood.
[4] D. Longo,et al. Differential in vitro and in vivo antitumor effects mediated by anti-CD40 and anti-CD20 monoclonal antibodies against human B-cell lymphomas. , 1996, Journal of immunotherapy with emphasis on tumor immunology : official journal of the Society for Biological Therapy.
[5] J Diebold,et al. Prognostic significance of bcl-2 protein expression in aggressive non-Hodgkin's lymphoma. Groupe d'Etude des Lymphomes de l'Adulte (GELA). , 1996, Blood.
[6] J C Reed,et al. Prognostic significance of Bcl-2 protein expression and Bcl-2 gene rearrangement in diffuse aggressive non-Hodgkin's lymphoma. , 1997, Blood.
[7] E. Vitetta,et al. Homodimerization of tumor-reactive monoclonal antibodies markedly increases their ability to induce growth arrest or apoptosis of tumor cells. , 1997, Proceedings of the National Academy of Sciences of the United States of America.
[8] A. Demidem,et al. Chimeric anti-CD20 (IDEC-C2B8) monoclonal antibody sensitizes a B cell lymphoma cell line to cell killing by cytotoxic drugs. , 1997, Cancer biotherapy & radiopharmaceuticals.
[9] W. Wilson,et al. Relationship of p53, bcl-2, and tumor proliferation to clinical drug resistance in non-Hodgkin's lymphomas. , 1997, Blood.
[10] D. Weisenburger,et al. Epidemiology of the non-Hodgkin's lymphomas: distributions of the major subtypes differ by geographic locations. Non-Hodgkin's Lymphoma Classification Project. , 1998, Annals of oncology : official journal of the European Society for Medical Oncology.
[11] J Hermans,et al. Clinical relevance of BCL2, BCL6, and MYC rearrangements in diffuse large B-cell lymphoma. , 1998, Blood.
[12] W. Kolch,et al. Suppression of Raf-1 kinase activity and MAP kinase signalling by RKIP , 1999, Nature.
[13] Meri,et al. Rituximab (Anti‐CD20) Therapy of B‐Cell Lymphomas: Direct Complement Killing is Superior to Cellular Effector Mechanisms , 2000, Scandinavian journal of immunology.
[14] Ash A. Alizadeh,et al. Ongoing immunoglobulin somatic mutation in germinal center B cell-like but not in activated B cell-like diffuse large cell lymphomas. , 2000, Proceedings of the National Academy of Sciences of the United States of America.
[15] W. Kolch,et al. Mechanism of Suppression of the Raf/MEK/Extracellular Signal-Regulated Kinase Pathway by the Raf Kinase Inhibitor Protein , 2000, Molecular and Cellular Biology.
[16] Ash A. Alizadeh,et al. Distinct types of diffuse large B-cell lymphoma identified by gene expression profiling , 2000, Nature.
[17] T. Sauerbruch,et al. Mechanism of cytotoxicity induced by chimeric mouse human monoclonal antibody IDEC-C2B8 in CD20-expressing lymphoma cell lines. , 2000, Cellular immunology.
[18] L. Presta,et al. Inhibitory Fc receptors modulate in vivo cytoxicity against tumor targets , 2000, Nature Medicine.
[19] T. Barbui,et al. CD20 levels determine the in vitro susceptibility to rituximab and complement of B-cell chronic lymphocytic leukemia: further regulation by CD55 and CD59. , 2001, Blood.
[20] B. Bonavida,et al. Inhibition of interleukin 10 by rituximab results in down-regulation of bcl-2 and sensitization of B-cell non-Hodgkin's lymphoma to apoptosis. , 2001, Clinical cancer research : an official journal of the American Association for Cancer Research.
[21] A. López-Guillermo,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. , 2001, Blood.
[22] B. Bonavida,et al. Rituximab inactivates signal transducer and activation of transcription 3 (STAT3) activity in B-non-Hodgkin's lymphoma through inhibition of the interleukin 10 autocrine/paracrine loop and results in down-regulation of Bcl-2 and sensitization to cytotoxic drugs. , 2001, Cancer research.
[23] Ulrich Siebenlist,et al. Constitutive Nuclear Factor κB Activity Is Required for Survival of Activated B Cell–like Diffuse Large B Cell Lymphoma Cells , 2001, The Journal of experimental medicine.
[24] W. Kolch,et al. Raf Kinase Inhibitor Protein Interacts with NF-κB-Inducing Kinase and TAK1 and Inhibits NF-κB Activation , 2001, Molecular and Cellular Biology.
[25] W. Weng,et al. Expression of complement inhibitors CD46, CD55, and CD59 on tumor cells does not predict clinical outcome after rituximab treatment in follicular non-Hodgkin lymphoma. , 2001, Blood.
[26] E. Vitetta,et al. 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. , 2001, Blood.
[27] Todd,et al. Diffuse large B-cell lymphoma outcome prediction by gene-expression profiling and supervised machine learning , 2002, Nature Medicine.
[28] G. Gaidano,et al. Acquired immunodeficiency syndrome‐associated lymphomas are efficiently lysed through complement‐dependent cytotoxicity and antibody‐dependent cellular cytotoxicity by rituximab , 2002, British journal of haematology.
[29] S. Barrans,et al. Germinal center phenotype and bcl-2 expression combined with the International Prognostic Index improves patient risk stratification in diffuse large B-cell lymphoma. , 2002, Blood.
[30] L. Staudt,et al. The use of molecular profiling to predict survival after chemotherapy for diffuse large-B-cell lymphoma. , 2002, The New England journal of medicine.
[31] Ash A. Alizadeh,et al. The t(14;18) defines a unique subset of diffuse large B-cell lymphoma with a germinal center B-cell gene expression profile. , 2002, Blood.
[32] B. E. C. Oiffier,et al. CHOP Chemotherapy plus Rituximab Compared with CHOP Alone in Elderly Patients with Diffuse Large-B-Cell Lymphoma , 2002 .
[33] T. Golub,et al. The molecular signature of mediastinal large B-cell lymphoma differs from that of other diffuse large B-cell lymphomas and shares features with classical Hodgkin lymphoma. , 2003, Blood.
[34] P. Gaulard,et al. Rituximab plus CHOP (R-CHOP) overcomes bcl-2--associated resistance to chemotherapy in elderly patients with diffuse large B-cell lymphoma (DLBCL). , 2003, Blood.
[35] A. Kennedy,et al. An anti-C3b(i) mAb enhances complement activation, C3b(i) deposition, and killing of CD20+ cells by rituximab. , 2003, Blood.
[36] Adrian Wiestner,et al. A gene expression-based method to diagnose clinically distinct subgroups of diffuse large B cell lymphoma , 2003, Proceedings of the National Academy of Sciences of the United States of America.
[37] L. Staudt,et al. Molecular Diagnosis of Primary Mediastinal B Cell Lymphoma Identifies a Clinically Favorable Subgroup of Diffuse Large B Cell Lymphoma Related to Hodgkin Lymphoma , 2003, The Journal of experimental medicine.
[38] R. Gressin,et al. In vitro mechanisms of action of rituximab on primary non-Hodgkin lymphomas. , 2003, Blood.
[39] 謙 大間知. CHOP chemotherapy plus rituximab compared with CHOP alone in elderly patients with diffuse large-B-cell lymphoma.Coiffier B,et al.N Engl J Med 2002;346(4):235-42--CHOP+リツキシマブ併用療法は、CHOP療法を上回る治療法であり、DLBCLの治療動向に大きなimpactを与えた , 2004 .
[40] B. Bonavida,et al. Rituximab inhibits p38 MAPK activity in 2F7 B NHL and decreases IL-10 transcription: Pivotal role of p38 MAPK in drug resistance , 2004, Oncogene.
[41] L. Goodglick,et al. Raf-1 kinase inhibitor protein: structure, function, regulation of cell signaling, and pivotal role in apoptosis. , 2004, Advances in cancer research.
[42] L. Staudt,et al. Confirmation of the molecular classification of diffuse large B-cell lymphoma by immunohistochemistry using a tissue microarray. , 2004, Blood.
[43] R. Rosenquist,et al. Evaluation of immunophenotype in diffuse large B-cell lymphoma and its impact on prognosis , 2005, Modern Pathology.
[44] R. Gascoyne,et al. Introduction of combined CHOP plus rituximab therapy dramatically improved outcome of diffuse large B-cell lymphoma in British Columbia. , 2005, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.
[45] P. Gaulard,et al. Long-term results of the R-CHOP study in the treatment of elderly patients with diffuse large B-cell lymphoma: a study by the Groupe d'Etude des Lymphomes de l'Adulte. , 2005, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.
[46] Y. Bang,et al. Improved therapeutic outcomes of DLBCL after introduction of rituximab in Korean patients , 2006, Annals of Hematology.
[47] S. Romano,et al. CD10 and Bcl‐2 expression combined with the International Prognostic Index can identify subgroups of patients with diffuse large‐cell lymphoma with very good or very poor prognoses , 2005, Histopathology.
[48] B. Bonavida,et al. Cellular and molecular signal transduction pathways modulated by rituximab (rituxan, anti-CD20 mAb) in non-Hodgkin's lymphoma: implications in chemosensitization and therapeutic intervention , 2005, Oncogene.
[49] P. De Baetselier,et al. Identification of a common gene signature for type II cytokine-associated myeloid cells elicited in vivo in different pathologic conditions. , 2006, Blood.
[50] S. Tomoyasu,et al. Treatment Effect of Rituximab Plus Chemotherapy Is Obtained by Improving Survival from Non-Germinal Center-Type Untreated Diffuse Large B-Cell Lymphoma. , 2006 .
[51] L. Staudt,et al. BCL2 expression is a prognostic marker for the activated B-cell-like type of diffuse large B-cell lymphoma. , 2006, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.
[52] W. Chan,et al. Mutational analysis of PRDM1 indicates a tumor-suppressor role in diffuse large B-cell lymphomas. , 2006, Blood.
[53] E. Schuuring,et al. Prognostic impact of germinal center-associated proteins and chromosomal breakpoints in poor-risk diffuse large B-cell lymphoma. , 2006, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.
[54] Stefano Monti,et al. Inactivation of the PRDM1/BLIMP1 gene in diffuse large B cell lymphoma , 2006, The Journal of experimental medicine.
[55] Randy D Gascoyne,et al. Rituximab-CHOP versus CHOP alone or with maintenance rituximab in older patients with diffuse large B-cell lymphoma. , 2006, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.
[56] A. López-Guillermo,et al. CHOP-like chemotherapy plus rituximab versus CHOP-like chemotherapy alone in young patients with good-prognosis diffuse large-B-cell lymphoma: a randomised controlled trial by the MabThera International Trial (MInT) Group. , 2006, The Lancet. Oncology.
[57] J. Armitage,et al. Bcl-2 gene expression as a predictor of outcome in diffuse large B-cell lymphoma. , 2006, Clinical lymphoma & myeloma.
[58] C J L M Meijer,et al. Immunohistochemical profiling based on Bcl‐2, CD10 and MUM1 expression improves risk stratification in patients with primary nodal diffuse large B cell lymphoma , 2006, The Journal of pathology.
[59] R. Gascoyne,et al. Addition of Rituximab (R) to CHOP Improves Survival in the Non-GCB Subtype of Diffuse Large B Cell Lymphoma (DLBCL). , 2006 .
[60] R. Gascoyne,et al. CHOP-R therapy overcomes the adverse prognostic influence of BCL-2 expression in diffuse large B-cell lymphoma , 2007, Leukemia & lymphoma.
[61] L. Staudt,et al. Gene Expression Signatures Predict Overall Survial in Diffuse Large B Cell Lymphoma Treated with Rituximab and Chop-Like Chemotherapy. , 2007 .
[62] T. Molina,et al. Germinal Center Phenotype Determined by Immunohistochemistry on Tissue Microarray Does Not Correlate with Outcome in Diffuse Large B-Cell Lymphoma Patients Treated with Immunochemotherapy in the Randomized Trial LNH98-5. A GELA Study. , 2007 .
[63] Andrew Lister,et al. Immunohistochemical prognostic markers in diffuse large B-cell lymphoma: validation of tissue microarray as a prerequisite for broad clinical applications--a study from the Lunenburg Lymphoma Biomarker Consortium. , 2007, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.
[64] U. Martens,et al. Immunophenotype as prognostic factor for diffuse large B-cell lymphoma in patients undergoing clinical risk-adapted therapy. , 2007, Annals of oncology : official journal of the European Society for Medical Oncology.
[65] Carl Blomqvist,et al. Prognostic impact of immunohistochemically defined germinal center phenotype in diffuse large B-cell lymphoma patients treated with immunochemotherapy. , 2007, Blood.
[66] David W. Hosmer,et al. Applied Survival Analysis: Regression Modeling of Time-to-Event Data , 2008 .
[67] A Rosenwald,et al. Retracted: Immunohistochemical prognostic markers in diffuse large B-cell lymphoma: validation of tissue microarray as a prerequisite for broad clinical applications (a study from the Lunenburg Lymphoma Biomarker Consortium) , 2007, Journal of Clinical Pathology.