Louis M Staudt

Summary

Affiliation: National Institutes of Health
Country: USA

Publications

  1. pmc Molecular diagnosis of primary mediastinal B cell lymphoma identifies a clinically favorable subgroup of diffuse large B cell lymphoma related to Hodgkin lymphoma
    Andreas Rosenwald
    Metabolism Branch, National Cancer Institute, National Institute of Health, Bethesda, MD 20892, USA
    J Exp Med 198:851-62. 2003
  2. pmc Aberrant immunoglobulin class switch recombination and switch translocations in activated B cell-like diffuse large B cell lymphoma
    Georg Lenz
    Metabolism Branch, Division of Cancer Treatment and Diagnosis, National Cancer Institute NCI, National Institutes of Health NIH, Bethesda, MD 20892, USA
    J Exp Med 204:633-43. 2007
  3. pmc Constitutive nuclear factor kappaB activity is required for survival of activated B cell-like diffuse large B cell lymphoma cells
    R E Davis
    Metabolism Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892-1374, USA
    J Exp Med 194:1861-74. 2001
  4. pmc Functional studies of BCL11A: characterization of the conserved BCL11A-XL splice variant and its interaction with BCL6 in nuclear paraspeckles of germinal center B cells
    Hui Liu
    Section of Molecular Genetics and Microbiology and Institute for Cellular and Molecular Biology, 1 University Station, A5000, University of Texas, Austin, Texas 78712, USA
    Mol Cancer 5:18. 2006
  5. pmc Distinct gene expression profiles in different B-cell compartments in human peripheral lymphoid organs
    Yulei Shen
    Department of Pathology, Eppley Cancer Institute, University of Nebraska Medical Center, Omaha, NE, USA
    BMC Immunol 5:20. 2004
  6. pmc Three microarray platforms: an analysis of their concordance in profiling gene expression
    David Petersen
    Advanced Technology Center, Center for Cancer Research, National Cancer Institute, Gaithersburg, MD 20877, USA
    BMC Genomics 6:63. 2005
  7. pmc Oncogenic activation of NF-kappaB
    Louis M Staudt
    Metabolism Branch, Center for Cancer Research, National Cancer Institute NIH, Bethesda, MD 20892 8322, USA
    Cold Spring Harb Perspect Biol 2:a000109. 2010
  8. ncbi request reprint Gene expression profiling of lymphoid malignancies
    Louis M Staudt
    Metabolism Branch, Center for Cancer Research, National Cancer Institute, 9000 Rockville Pike, Bethesda, Maryland 20892, USA
    Annu Rev Med 53:303-18. 2002
  9. pmc Molecular subtypes of diffuse large B-cell lymphoma arise by distinct genetic pathways
    Georg Lenz
    Metabolism Branch, Biometric Research Branch, Center for Information Technology, and Laboratory of Pathology, Center for Cancer Research, National Cancer Institute, Bethesda, MD 20892, USA
    Proc Natl Acad Sci U S A 105:13520-5. 2008
  10. ncbi request reprint Molecular diagnosis of the hematologic cancers
    Louis M Staudt
    Metabolism Branch, Center for Cancer Research, National Cancer Institute, Bethesda, MD 20892, USA
    N Engl J Med 348:1777-85. 2003

Detail Information

Publications98

  1. pmc Molecular diagnosis of primary mediastinal B cell lymphoma identifies a clinically favorable subgroup of diffuse large B cell lymphoma related to Hodgkin lymphoma
    Andreas Rosenwald
    Metabolism Branch, National Cancer Institute, National Institute of Health, Bethesda, MD 20892, USA
    J Exp Med 198:851-62. 2003
    ..The molecular diagnosis of PMBL should significantly aid in the development of therapies tailored to this clinically and pathogenetically distinctive subgroup of DLBCL...
  2. pmc Aberrant immunoglobulin class switch recombination and switch translocations in activated B cell-like diffuse large B cell lymphoma
    Georg Lenz
    Metabolism Branch, Division of Cancer Treatment and Diagnosis, National Cancer Institute NCI, National Institutes of Health NIH, Bethesda, MD 20892, USA
    J Exp Med 204:633-43. 2007
    ..Accordingly, aberrant switch recombination was responsible for translocations in ABC DLBCLs involving BCL6, MYC, and a novel translocation partner, SPIB...
  3. pmc Constitutive nuclear factor kappaB activity is required for survival of activated B cell-like diffuse large B cell lymphoma cells
    R E Davis
    Metabolism Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892-1374, USA
    J Exp Med 194:1861-74. 2001
    ....
  4. pmc Functional studies of BCL11A: characterization of the conserved BCL11A-XL splice variant and its interaction with BCL6 in nuclear paraspeckles of germinal center B cells
    Hui Liu
    Section of Molecular Genetics and Microbiology and Institute for Cellular and Molecular Biology, 1 University Station, A5000, University of Texas, Austin, Texas 78712, USA
    Mol Cancer 5:18. 2006
    ..Chromosomal aberrations of BCL11A at 2p16.1 have been reported in a variety of B-cell malignancies and its deficiency in mice leads to a profound block in B-cell development...
  5. pmc Distinct gene expression profiles in different B-cell compartments in human peripheral lymphoid organs
    Yulei Shen
    Department of Pathology, Eppley Cancer Institute, University of Nebraska Medical Center, Omaha, NE, USA
    BMC Immunol 5:20. 2004
    ..The B-cell maturational process is accompanied by changes in the expression of cell-surface and intracellular proteins and requires signals from the specialized microenvironments...
  6. pmc Three microarray platforms: an analysis of their concordance in profiling gene expression
    David Petersen
    Advanced Technology Center, Center for Cancer Research, National Cancer Institute, Gaithersburg, MD 20877, USA
    BMC Genomics 6:63. 2005
    ..As part of a validation study for the long oligonucleotide arrays, we compared and contrasted expression profiles from the three formats, testing RNA from six different cell lines against a universal reference standard...
  7. pmc Oncogenic activation of NF-kappaB
    Louis M Staudt
    Metabolism Branch, Center for Cancer Research, National Cancer Institute NIH, Bethesda, MD 20892 8322, USA
    Cold Spring Harb Perspect Biol 2:a000109. 2010
    ..Inhibition of constitutive NF-kappaB signaling in each of these cancer types induces apoptosis, providing a rationale for the development of NF-kappaB pathway inhibitors for the treatment of cancer...
  8. ncbi request reprint Gene expression profiling of lymphoid malignancies
    Louis M Staudt
    Metabolism Branch, Center for Cancer Research, National Cancer Institute, 9000 Rockville Pike, Bethesda, Maryland 20892, USA
    Annu Rev Med 53:303-18. 2002
    ..Gene expression analysis also illuminated the mechanism of lymphomagenesis caused by BCL-6 translocations and provided evidence that the NF-kappa B signaling pathway is a new molecular therapeutic target in DLBCL...
  9. pmc Molecular subtypes of diffuse large B-cell lymphoma arise by distinct genetic pathways
    Georg Lenz
    Metabolism Branch, Biometric Research Branch, Center for Information Technology, and Laboratory of Pathology, Center for Cancer Research, National Cancer Institute, Bethesda, MD 20892, USA
    Proc Natl Acad Sci U S A 105:13520-5. 2008
    ..Together, these data provide genetic evidence that the DLBCL subtypes are distinct diseases that use different oncogenic pathways...
  10. ncbi request reprint Molecular diagnosis of the hematologic cancers
    Louis M Staudt
    Metabolism Branch, Center for Cancer Research, National Cancer Institute, Bethesda, MD 20892, USA
    N Engl J Med 348:1777-85. 2003
  11. ncbi request reprint Focus on lymphomas
    Louis M Staudt
    Metabolism Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA
    Cancer Cell 2:363-6. 2002
  12. pmc IRF4 addiction in multiple myeloma
    Arthur L Shaffer
    Metabolism Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA
    Nature 454:226-31. 2008
    ..Although IRF4 is not genetically altered in most myelomas, they are nonetheless addicted to an aberrant IRF4 regulatory network that fuses the gene expression programmes of normal plasma cells and activated B cells...
  13. pmc Compensatory IKKalpha activation of classical NF-kappaB signaling during IKKbeta inhibition identified by an RNA interference sensitization screen
    Lloyd T Lam
    Metabolism Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA
    Proc Natl Acad Sci U S A 105:20798-803. 2008
    ..These results suggest that therapy for ABC DLBCL may be improved by targeting both IKKalpha and IKKbeta, possibly through CARD11 inhibition...
  14. ncbi request reprint Molecular diagnosis of Burkitt's lymphoma
    Sandeep S Dave
    National Cancer Institute, National Institutes of Health, Bethesda, MD, USA
    N Engl J Med 354:2431-42. 2006
    ..We examined whether gene-expression profiling could reliably distinguish Burkitt's lymphoma from diffuse large-B-cell lymphoma...
  15. pmc Casein kinase 1alpha governs antigen-receptor-induced NF-kappaB activation and human lymphoma cell survival
    Nicolas Bidere
    Molecular Development Section, Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA
    Nature 458:92-6. 2009
    ..ABC DLBCL cells required CK1alpha for constitutive NF-kappaB activity, indicating that CK1alpha functions as a conditionally essential malignancy gene-a member of a new class of potential cancer therapeutic targets...
  16. ncbi request reprint The proliferation gene expression signature is a quantitative integrator of oncogenic events that predicts survival in mantle cell lymphoma
    Andreas Rosenwald
    The Lymphoma Leukemia Molecular Profiling Project, National Cancer Institute NIH, Bethesda, MD, USA
    Cancer Cell 3:185-97. 2003
    ..We propose a quantitative model of the aberrant cell cycle regulation in MCL that provides a rationale for the design of cell cycle inhibitor therapy in this malignancy...
  17. ncbi request reprint A loss-of-function RNA interference screen for molecular targets in cancer
    Vu N Ngo
    Metabolism Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA
    Nature 441:106-10. 2006
    ..The methodology that we describe can be used to establish a functional taxonomy of cancer and help reveal new classes of therapeutic targets distinct from known oncogenes...
  18. ncbi request reprint Low-intensity therapy in adults with Burkitt's lymphoma
    Kieron Dunleavy
    From the Center for Cancer Research, National Cancer Institute, Bethesda, MD
    N Engl J Med 369:1915-25. 2013
    ..Current treatments are less effective and have more severe side effects in adults and patients with immunodeficiency than in children...
  19. ncbi request reprint XBP1, downstream of Blimp-1, expands the secretory apparatus and other organelles, and increases protein synthesis in plasma cell differentiation
    A L Shaffer
    Metabolism Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, 9000 Rockville Pike, Bethesda, MD 20892, USA
    Immunity 21:81-93. 2004
    ..Thus, XBP1 coordinates diverse changes in cellular structure and function resulting in the characteristic phenotype of professional secretory cells...
  20. ncbi request reprint Prediction of survival in follicular lymphoma based on molecular features of tumor-infiltrating immune cells
    Sandeep S Dave
    National Cancer Institute, NIH, Bethesda, MD 20892, USA
    N Engl J Med 351:2159-69. 2004
    ..We used gene-expression profiles of tumor-biopsy specimens obtained at diagnosis to develop a molecular predictor of the length of survival...
  21. pmc Frequent engagement of the classical and alternative NF-kappaB pathways by diverse genetic abnormalities in multiple myeloma
    Christina M Annunziata
    Metabolism Branch, Center for Cancer Research, National Cancer Institute, Bethesda, MD 20892, USA
    Cancer Cell 12:115-30. 2007
    ..These data demonstrate that addiction to the NF-kappaB pathway is frequent in myeloma and suggest that IKKbeta inhibitors hold promise for the treatment of this disease...
  22. pmc Cooperative signaling through the signal transducer and activator of transcription 3 and nuclear factor-{kappa}B pathways in subtypes of diffuse large B-cell lymphoma
    Lloyd T Lam
    Metabolism Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA
    Blood 111:3701-13. 2008
    ..These findings suggest that the biological interplay between the STAT3 and NF-kappaB pathways may be exploited for the treatments of a subset of ABC DLBCLs...
  23. pmc Burkitt lymphoma pathogenesis and therapeutic targets from structural and functional genomics
    Roland Schmitz
    Metabolism Branch Center for Cancer Research, National Cancer Institute, NIH, Bethesda, Maryland 20892, USA
    Nature 490:116-20. 2012
    ..In 38% of sporadic BL cases, oncogenic CCND3 mutations produced highly stable cyclin D3 isoforms that drive cell cycle progression. These findings suggest opportunities to improve therapy for patients with BL...
  24. ncbi request reprint Exploiting synthetic lethality for the therapy of ABC diffuse large B cell lymphoma
    Yibin Yang
    Metabolism Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA
    Cancer Cell 21:723-37. 2012
    ..Blockade of B cell receptor signaling using the BTK inhibitor ibrutinib also downregulates IRF4 and consequently synergizes with lenalidomide in killing ABC DLBCLs, suggesting attractive therapeutic strategies...
  25. pmc Chronic active B-cell-receptor signalling in diffuse large B-cell lymphoma
    R Eric Davis
    Metabolism Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA
    Nature 463:88-92. 2010
    ..These findings establish chronic active BCR signalling as a new pathogenetic mechanism in ABC DLBCL, suggesting several therapeutic strategies...
  26. ncbi request reprint Overexpression of c-maf is a frequent oncogenic event in multiple myeloma that promotes proliferation and pathological interactions with bone marrow stroma
    Elaine M Hurt
    Metabolism Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA
    Cancer Cell 5:191-9. 2004
    ..The frequent overexpression of c-maf in myeloma makes it an attractive target for therapeutic intervention...
  27. doi request reprint Oncogenic CARD11 mutations in human diffuse large B cell lymphoma
    Georg Lenz
    Metabolism Branch, Division of Cancer Treatment and Diagnosis, Center for Cancer Research, National Cancer Institute, Bethesda, MD 20892, USA
    Science 319:1676-9. 2008
    ..These results demonstrate that CARD11 is a bona fide oncogenein DLBCL, providing a genetic rationale for the development of pharmacological inhibitors of the CARD11 pathway for DLBCL therapy...
  28. ncbi request reprint A library of gene expression signatures to illuminate normal and pathological lymphoid biology
    Arthur L Shaffer
    Metabolism Branch, Center for Cancer Research, National Cancer Institute, Bethesda, MD 20892, USA
    Immunol Rev 210:67-85. 2006
    ..We also discuss the use of genomic-scale RNAi libraries to identify genes and pathways that may serve as therapeutic targets in B-cell malignancies...
  29. ncbi request reprint Blimp-1 orchestrates plasma cell differentiation by extinguishing the mature B cell gene expression program
    A L Shaffer
    Metabolism Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA
    Immunity 17:51-62. 2002
    ....
  30. doi request reprint Oncogenically active MYD88 mutations in human lymphoma
    Vu N Ngo
    Metabolism Branch, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, Maryland 20892, USA
    Nature 470:115-9. 2011
    ....
  31. pmc A mechanistic rationale for MEK inhibitor therapy in myeloma based on blockade of MAF oncogene expression
    Christina M Annunziata
    Metabolism Branch, Center for Cancer Research, National Cancer Institute, 10 Center Dr, Bethesda, MD 20892 1374, USA
    Blood 117:2396-404. 2011
    ..The data presented herein demonstrate that the MEK-ERK pathway regulates MAF transcription, providing molecular rationale for clinical evaluation of MEK inhibitors in MAF-expressing myeloma...
  32. pmc Differential efficacy of bortezomib plus chemotherapy within molecular subtypes of diffuse large B-cell lymphoma
    Kieron Dunleavy
    Center for Cancer Research, National Cancer Institute, Bethesda, MD 20892, USA
    Blood 113:6069-76. 2009
    ..This trial is registered with http://www.ClinicalTrials.gov under identifier NCT00057902...
  33. pmc Point mutations and genomic deletions in CCND1 create stable truncated cyclin D1 mRNAs that are associated with increased proliferation rate and shorter survival
    Adrian Wiestner
    Center for Cancer Research, National Cancer Institute, National Institutes of Health, 9000 Rockville Pike, Bethesda, MD 20892, USA
    Blood 109:4599-606. 2007
    ..We conclude that alterations of CCND1 3'UTR structure can significantly increase its oncogenic effect and worsen the clinical course of MCL patients...
  34. pmc The biology of human lymphoid malignancies revealed by gene expression profiling
    Louis M Staudt
    Metabolism Branch, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, Maryland 20892, USA
    Adv Immunol 87:163-208. 2005
    ..The implications of these insights for the diagnosis and treatment of non-Hodgkin lymphomas are discussed...
  35. pmc Two newly characterized germinal center B-cell-associated genes, GCET1 and GCET2, have differential expression in normal and neoplastic B cells
    Zenggang Pan
    Department of Pathology and Microbiology, University of Nebraska Medical Center, Omaha, Nebraska and The Metabolism Branch, National Cancer Institute, Bethesda, Maryland, USA
    Am J Pathol 163:135-44. 2003
    ..Multiple markers are necessary to differentiate the GCB from the activated B-cell type of diffuse large B-cell lymphoma with a high degree of accuracy...
  36. pmc A gene expression-based method to diagnose clinically distinct subgroups of diffuse large B cell lymphoma
    George Wright
    Biometric Research Branch, Division of Cancer Treatment and Diagnosis, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA
    Proc Natl Acad Sci U S A 100:9991-6. 2003
    ..These results demonstrate the ability of this gene expression-based predictor to classify DLBCLs into biologically and clinically distinct subgroups irrespective of the method used to measure gene expression...
  37. ncbi request reprint Control of autophagic cell death by caspase-10 in multiple myeloma
    Laurence Lamy
    Metabolism Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, 9000 Rockville Pike, Bethesda, MD 20892, USA
    Cancer Cell 23:435-49. 2013
    ..While myeloma cells require a basal level of autophagy for survival, caspase-10 tempers this response to avoid cell death. Drugs that disrupt this vital balance may have therapeutic potential in myeloma...
  38. pmc Congenital B cell lymphocytosis explained by novel germline CARD11 mutations
    Andrew L Snow
    Lymphocyte Molecular Genetics Unit, Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health NIH, Bethesda, MD 20892, USA
    J Exp Med 209:2247-61. 2012
    ....
  39. pmc Molecular and cytological features of the mouse B-cell lymphoma line iMycEmu-1
    Seong Su Han
    Laboratory of Genetics, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, MD, USA
    Mol Cancer 4:40. 2005
    ..The purpose of this study was to establish and characterize a cell line, designated iMycEmu-1, for the in-depth evaluation of LBL in vitro...
  40. ncbi request reprint Small molecule inhibitors of IkappaB kinase are selectively toxic for subgroups of diffuse large B-cell lymphoma defined by gene expression profiling
    Lloyd T Lam
    Metabolism Branch, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, Maryland, USA
    Clin Cancer Res 11:28-40. 2005
    ..These studies validate the NF-kappaB pathway as a promising therapeutic target in ABC DLBCL, PMBL, and other lymphomas that depend on the activity of NF-kappaB for survival and proliferation...
  41. ncbi request reprint The use of molecular profiling to predict survival after chemotherapy for diffuse large-B-cell lymphoma
    Andreas Rosenwald
    Metabolism Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA
    N Engl J Med 346:1937-47. 2002
    ..The survival of patients with diffuse large-B-cell lymphoma after chemotherapy is influenced by molecular features of the tumors. We used the gene-expression profiles of these lymphomas to develop a molecular predictor of survival...
  42. ncbi request reprint Analysis of gamma c-family cytokine target genes. Identification of dual-specificity phosphatase 5 (DUSP5) as a regulator of mitogen-activated protein kinase activity in interleukin-2 signaling
    Panu E Kovanen
    Laboratory of Molecular Immunology, NHLBI, National Institutes of Health, Maryland 20892, USA
    J Biol Chem 278:5205-13. 2003
    ..Our findings provide insights into the shared versus distinctive actions by different members of the gamma(c) family of cytokines. Moreover, we have identified a DUSP5-dependent negative regulatory pathway for MAPK activity in T cells...
  43. doi request reprint Dose-adjusted EPOCH-rituximab therapy in primary mediastinal B-cell lymphoma
    Kieron Dunleavy
    Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA
    N Engl J Med 368:1408-16. 2013
    ..We aimed to develop a strategy that improves the rate of cure and obviates the need for radiotherapy...
  44. ncbi request reprint Lymphoid malignancies: the dark side of B-cell differentiation
    A L Shaffer
    Metabolism Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA
    Nat Rev Immunol 2:920-32. 2002
    ..The similarities and differences between malignant and normal B cells indicate strategies for the treatment of these cancers...
  45. pmc Bortezomib resistance in mantle cell lymphoma is associated with plasmacytic differentiation
    Patricia Perez-Galan
    Hematology Branch, National Heart, Lung and Blood Institute, National Institutes of Health, Bethesda, MD, USA
    Blood 117:542-52. 2011
    ..Expression of CD38 and IRF4 could serve as markers of bortezomib resistance in MCL. This study has been registered at http://clinicaltrials.gov as NCT00131976...
  46. ncbi request reprint ZAP-70 expression identifies a chronic lymphocytic leukemia subtype with unmutated immunoglobulin genes, inferior clinical outcome, and distinct gene expression profile
    Adrian Wiestner
    Metabolism Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892
    Blood 101:4944-51. 2003
    ..We developed reverse transcriptase-polymerase chain reaction and immunohistochemical assays for ZAP-70 expression that can be applied clinically and would yield important prognostic information for patients with CLL...
  47. pmc Cooperative epigenetic modulation by cancer amplicon genes
    Lixin Rui
    Metabolism Branch, National Cancer Institute, Bethesda, MD 20892, USA
    Cancer Cell 18:590-605. 2010
    ..Hence, JAK2 and JMJD2C cooperatively remodel the PMBL and HL epigenome, offering a mechanistic rationale for the development of JAK2 and JMJD2C inhibitors in these diseases...
  48. ncbi request reprint Clinical translation of gene expression profiling in lymphomas and leukemias
    Andreas Rosenwald
    Metabolism Branch, Center for Cancer Research, National Cancer Institute, Bethesda, MD 20892, USA
    Semin Oncol 29:258-63. 2002
    ..As the armamentarium of molecularly targeted therapies expands, molecular diagnosis will be seen as an integral component of clinical management...
  49. ncbi request reprint Fludarabine treatment of patients with chronic lymphocytic leukemia induces a p53-dependent gene expression response
    Andreas Rosenwald
    Metabolism Branch, Center for Cancer Research, National Cancer Institute NIH, Bldg 10, Rm 4N114, Bethesda, MD 20892, USA
    Blood 104:1428-34. 2004
    ..These considerations suggest that fludarabine treatment should be given in strict accordance to the current National Cancer Institute (NCI) guidelines that have established criteria of disease activity that warrant treatment...
  50. doi request reprint Pathogenetic importance and therapeutic implications of NF-κB in lymphoid malignancies
    Kian Huat Lim
    Metabolism Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA
    Immunol Rev 246:359-78. 2012
    ..Fortunately, a number of drugs that block signaling cascades leading to NF-κB are in early phase clinical trials, several of which are already showing activity in lymphoid malignancies...
  51. doi request reprint Unique cell surface expression of receptor tyrosine kinase ROR1 in human B-cell chronic lymphocytic leukemia
    Sivasubramanian Baskar
    Experimental Transplantation and Immunology Branch and Metabolism Branch, Center for Cancer Research, National Cancer Institute, and Hematology Branch, National Heart, Lung and Blood Institute, NIH, Bethesda, MD 20892 1203, USA
    Clin Cancer Res 14:396-404. 2008
    ..To assess the suitability of ROR1 as a cell surface antigen for targeted therapy of B-CLL, we carried out a comprehensive analysis of ROR1 protein expression...
  52. ncbi request reprint Towards molecular diagnosis and targeted therapy of lymphoid malignancies
    Adrian Wiestner
    Metabolism Branch, Center for Cancer Research, National Cancer Institute, National Institute of Health, Bethesda, MD 20892, USA
    Semin Hematol 40:296-307. 2003
    ..The full benefit of gene expression profiling can only be realized if we incorporate this technology into prospective clinical trials...
  53. doi request reprint Pathogenesis of human B cell lymphomas
    Arthur L Shaffer
    Metabolism Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA
    Annu Rev Immunol 30:565-610. 2012
    ..These mechanistic insights are ushering in an era of targeted therapies for these cancers based on the principles of pathogenesis...
  54. ncbi request reprint The BCL-2 biomarker in the era of molecular diagnosis of diffuse large B-cell lymphoma
    Kieron Dunleavy
    Metabolism Branch, Center for Cancer Research, National Cancer Institute, Bethesda, MD, USA
    Leuk Lymphoma 48:1061-3. 2007
  55. ncbi request reprint A closer look at follicular lymphoma
    Louis M Staudt
    Metabolism Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA
    N Engl J Med 356:741-2. 2007
  56. ncbi request reprint Gene expression profiling of diffuse large B-cell lymphoma
    Andreas Rosenwald
    Metabolism Branch, Center for Cancer Research, National Cancer Institute, Building 10, 4N114, 9000 Rockville Pike, Bethesda, MD, USA
    Leuk Lymphoma 44:S41-7. 2003
    ..The use of gene expression profiling should eventually lead to an integration of molecular diagnosis and consequent selection of the most appropriate treatment...
  57. pmc IRF4: Immunity. Malignancy! Therapy?
    Arthur L Shaffer
    Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA
    Clin Cancer Res 15:2954-61. 2009
    ..Interference with IRF4 expression is lethal to multiple myeloma cells, irrespective of their genetic etiology, making IRF4 an "Achilles' heel" that may be exploited therapeutically...
  58. pmc Identification of FGFR4-activating mutations in human rhabdomyosarcomas that promote metastasis in xenotransplanted models
    James G Taylor
    Pulmonary and Vascular Medicine Branch, National Heart, Lung, and Blood Institute NHLBI, NIH, Bethesda, Maryland 20892 4605, USA
    J Clin Invest 119:3395-407. 2009
    ..These findings support the potential therapeutic targeting of FGFR4 in RMS...
  59. pmc Methylation profiling of mediastinal gray zone lymphoma reveals a distinctive signature with elements shared by classical Hodgkin's lymphoma and primary mediastinal large B-cell lymphoma
    Franziska C Eberle
    Laboratory of Pathology, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA
    Haematologica 96:558-66. 2011
    ..Epigenetic changes have been implicated in the loss of the B-cell program in classical Hodgkin's lymphoma, and might provide a basis for the immunophenotypic alterations seen in mediastinal gray zone lymphoma...
  60. doi request reprint Malignant pirates of the immune system
    Lixin Rui
    Metabolism Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA
    Nat Immunol 12:933-40. 2011
    ....
  61. ncbi request reprint Ribosomal protein S3: a KH domain subunit in NF-kappaB complexes that mediates selective gene regulation
    Fengyi Wan
    Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, Bethesda, MD 20892, USA
    Cell 131:927-39. 2007
    ..Our observations provide insight into how NF-kappaB selectively controls gene expression...
  62. doi request reprint Targeting pathological B cell receptor signalling in lymphoid malignancies
    Ryan M Young
    Metabolism Branch, Center for Cancer Research, National Cancer Institute, US National Institutes of Health, Bethesda, Maryland 20892, USA
    Nat Rev Drug Discov 12:229-43. 2013
    ..A host of therapeutic agents targeting effectors of the BCR signalling pathway are now in clinical trials and have shown initial success against multiple forms of lymphoma...
  63. pmc Identification of FoxM1/Bub1b signaling pathway as a required component for growth and survival of rhabdomyosarcoma
    Xiaolin Wan
    Molecular Oncology Section, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA
    Cancer Res 72:5889-99. 2012
    ..These results show the important role of the Bub1b/FoxM1 pathway in RMS and provide potential therapeutic targets...
  64. ncbi request reprint A cell-based assay for IkappaBalpha stabilization using a two-color dual luciferase-based sensor
    R Eric Davis
    Metabolism Branch, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, MD 20892 3370, USA
    Assay Drug Dev Technol 5:85-103. 2007
    ..Known and unexpected inhibitors of NFkappaB signaling were identified from the bioactive collection. We describe here the development and performance of this assay, and discuss the merits of its specific features...
  65. ncbi request reprint Molecular diagnosis of lymphoid malignancies by gene expression profiling
    R Eric Davis
    Metabolism Branch, Center for Cancer Research, National Cancer Institute, Bethesda, Maryland 20892, USA
    Curr Opin Hematol 9:333-8. 2002
    ....
  66. ncbi request reprint It's ALL in the diagnosis
    Louis M Staudt
    Metabolism Branch, Center for Cancer Research, National Cancer Institute, 9000 Rockville Pike, Bethesda, MD 20892, USA
    Cancer Cell 1:109-10. 2002
    ..Recent gene expression profiling studies of pediatric acute lymphoblastic leukemia (ALL) suggest that the molecular diagnosis of these diseases is right around the corner...
  67. ncbi request reprint Linking laboratory and clinical research: the development of molecularly targeted therapeutics inside the national cancer institute center for cancer research
    J Carl Barrett
    National Cancer Institute Center for Cancer Research, National Institutes of Health, Bethesda, MD 20892, USA
    Clin Adv Hematol Oncol 1:302-6. 2003
    ..Its infrastructure supports the iterative flow of information from the bench to the bedside and from the bedside to the bench, expediting the delivery of molecularly based therapeutics to cancer patients...
  68. doi request reprint Inhibitors of the NF-kappaB activation pathway from Cryptocarya rugulosa
    Tamara L Meragelman
    Screening Technologies Branch, Developmental Therapeutics Program, Division of Cancer Treatment and Diagnosis, National Cancer Institute, Frederick, Maryland, USA
    J Nat Prod 72:336-9. 2009
    ..Rugulactone was the more active compound, exhibiting up to 5-fold induction of IkappaB at 25 microg/mL; maximal activity was observed with 10 h exposure of test cells to 1 or 2...
  69. doi request reprint High-throughput RNA sequencing in B-cell lymphomas
    Wenming Xiao
    Bioinformatics and Molecular Analysis Section, Division of Computational Bioscience, Center for Information Technology, National Institutes of Health, Bethesda, MD, USA
    Methods Mol Biol 971:295-312. 2013
    ....
  70. ncbi request reprint Transformation of late passage insulin-like growth factor-I receptor null mouse embryo fibroblasts by SV40 T antigen
    Susan L Spence
    Metabolism Branch, National Cancer Institute, NIH, Bethesda, Maryland 20892, USA
    Cancer Res 66:4233-9. 2006
    ..We conclude that late passage IGF-I receptor null mouse embryo fibroblasts can be transformed by SV40 T antigen, and that ErbB-3 may play a role in permitting transformation by T antigen...
  71. doi request reprint A new "brew" of MALT1 inhibitors
    Ryan M Young
    Metabolism Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, 9000 Rockville Pike, Bethesda, MD 20892, USA
    Cancer Cell 22:706-7. 2012
    ..In this issue of Cancer Cell, Nagel and colleagues and Fontan and colleagues describe MALT1 inhibitors suitable for clinical use that are selectively toxic to this malignancy...
  72. ncbi request reprint Insertion of Myc into Igh accelerates peritoneal plasmacytomas in mice
    Sung Sup Park
    Laboratory of Genetics, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, Maryland 20892 4256, USA
    Cancer Res 65:7644-52. 2005
    ....
  73. ncbi request reprint MALT1 is deregulated by both chromosomal translocation and amplification in B-cell non-Hodgkin lymphoma
    Dolors Sanchez-Izquierdo
    Department of Hematology and Medical Oncology, Hospital Clinico, University of Valencia, Spain
    Blood 101:4539-46. 2003
    ..Together, these data implicate MALT1 as a dominant oncogene that may play a role in the pathogenesis of B-NHL...
  74. pmc Structural profiles of TP53 gene mutations predict clinical outcome in diffuse large B-cell lymphoma: an international collaborative study
    Ken H Young
    Department of Pathology and Laboratory Medicine, University of Wisconsin School of Medicine and Public Health, University of of Wisconsin Paul P Carbone Comprehensive Cancer Center, Madison, USA
    Blood 112:3088-98. 2008
    ..This study shows the prognostic importance of mutations in the TP53 DNA-binding domains in patients with DLBCL...
  75. ncbi request reprint MALT1 and the API2-MALT1 fusion act between CD40 and IKK and confer NF-kappa B-dependent proliferative advantage and resistance against FAS-induced cell death in B cells
    Liza Ho
    Department of Clinical Pathology, Geneva University Hospital, Centre Medical Universitaire, Geneva, Switzerland
    Blood 105:2891-9. 2005
    ..Our findings support a model in which NF-kappa B signaling, once activated in a CD40-dependent immune response, is maintained and enhanced through deregulation of MALT1 or formation of an API2-MALT1 fusion...
  76. ncbi request reprint Cancer: negative feedback for B cells
    Louis M Staudt
    Nature 431:919-20. 2004
  77. ncbi request reprint Direct repression of prdm1 by Bcl-6 inhibits plasmacytic differentiation
    Chainarong Tunyaplin
    Department of Microbiology, Columbia University College of Physicians and Surgeons, New York, NY 10032, USA
    J Immunol 173:1158-65. 2004
    ..These mice have elevated Ab response, increased Ig-secreting cells, and increased Blimp-1(+) cells in spleen following immunization and their splenic B cells show accelerated plasmacytic development in vitro...
  78. ncbi request reprint Comprehensive whole genome array CGH profiling of mantle cell lymphoma model genomes
    Ronald J de Leeuw
    Department of Cancer Genetics, British Columbia Cancer Agency, Vancouver, BC, Canada
    Hum Mol Genet 13:1827-37. 2004
    ..Further characterization of such minimally altered genomic regions identified using whole genome array CGH will define novel dominant oncogenes and tumor suppressor genes that play important roles in the pathogenesis of MCL...
  79. pmc BCL2 translocation defines a unique tumor subset within the germinal center B-cell-like diffuse large B-cell lymphoma
    Javeed Iqbal
    Department of Pathology and Microbiology, University of Nebraska Medical Center, 983135 Nebraska Medical Center, Omaha, NE 68198 3135, USA
    Am J Pathol 165:159-66. 2004
    ..However, despite this higher proliferative activity, there was no significant difference in overall or failure-free survival between the t(14;18)-positive and -negative subsets within the GCB subgroup...
  80. pmc Role of NF-kappa B in cell survival and transcription of latent membrane protein 1-expressing or Epstein-Barr virus latency III-infected cells
    Ellen D Cahir-McFarland
    The Channing Laboratory and Infectious Disease Division, Brigham and Women s Hospital, and Department of Medicine, Harvard Medical School, Boston, Massachusetts 02115, USA
    J Virol 78:4108-19. 2004
    ..Expression of IRF-2, AIM1, ASK1, SNF2L2, and components of IFN signaling pathways further distinguished EBV latency III-infected B cells from IgM-stimulated or germinal-center B cells...
  81. ncbi request reprint Loss of MHC class II gene and protein expression in diffuse large B-cell lymphoma is related to decreased tumor immunosurveillance and poor patient survival regardless of other prognostic factors: a follow-up study from the Leukemia and Lymphoma Molecular
    Lisa M Rimsza
    Department of Pathology, College of Medicine, University of Arizona, 1501 N Campbell Ave, PO Box 245043, Tucson, AZ 85724 5043, USA
    Blood 103:4251-8. 2004
    ..8% versus 11.0%; P =.001), supporting the hypothesis that loss of tumor immunosurveillance has a devastating effect on patient outcome in DLBCL...
  82. ncbi request reprint ZAP-70 expression and prognosis in chronic lymphocytic leukaemia
    Jenny A Orchard
    Department of Haematology, Royal Bournemouth Hospital, Bournemouth, UK
    Lancet 363:105-11. 2004
    ..We assessed whether ZAP-70 could be used as a prognostic marker in CLL...
  83. pmc Growth suppression by acute promyelocytic leukemia-associated protein PLZF is mediated by repression of c-myc expression
    Melanie J McConnell
    Division of Hematology Oncology, Department of Medicine, Mount Sinai School of Medicine, One Gustave L Levy Place, New York, NY 10029, USA
    Mol Cell Biol 23:9375-88. 2003
    ..Loss of this repression through the translocation that occurs in t(11;17) would have serious consequences for cell growth control...
  84. ncbi request reprint The t(14;18) defines a unique subset of diffuse large B-cell lymphoma with a germinal center B-cell gene expression profile
    James Z Huang
    Department of Pathology, The Munroe Meyer Institute for Genetics and Rehabilitation, University of Nebraska Medical Center, Omaha, NE 68198, USA
    Blood 99:2285-90. 2002
    ..CD10 protein expression is useful in identifying cases of DLBCL with a germinal center B-cell gene expression profile and is often expressed in cases with the t(14;18)...
  85. ncbi request reprint Characterization of 8p21.3 chromosomal deletions in B-cell lymphoma: TRAIL-R1 and TRAIL-R2 as candidate dosage-dependent tumor suppressor genes
    Fanny Rubio-Moscardo
    Center for Applied Medical Research CIMA, Division of Oncology, University of Navarra, Avda Pio XII, 55, Pamplona 31008, Spain
    Blood 106:3214-22. 2005
    ..Our data suggest that TRAIL-R1 and TRAIL-R2 act as dosage-dependent tumor suppressor genes whose monoallelic deletion can impair TRAIL-induced apoptosis in B-cell lymphoma...
  86. ncbi request reprint BCL2 expression is a prognostic marker for the activated B-cell-like type of diffuse large B-cell lymphoma
    Javeed Iqbal
    Leukemia Lymphoma Molecular Profiling Project, Department of Pathology and Microbiology, University of Nebraska Medical Center, Omaha, NE 68198 3135, USA
    J Clin Oncol 24:961-8. 2006
    ..DLBCL is heterogeneous, and the expression of BCL2 is variable within the two major subgroups of DLBCL, germinal center B-cell-like (GCB) and activated B-cell-like (ABC) DLBCL, as well as primary mediastinal DLBCL...
  87. pmc Mutation and genomic deletion status of ataxia telangiectasia mutated (ATM) and p53 confer specific gene expression profiles in mantle cell lymphoma
    Timothy C Greiner
    Department of Pathology and Microbiology, University of Nebraska Medical Center, Omaha, NE 68198, USA
    Proc Natl Acad Sci U S A 103:2352-7. 2006
    ..This information on molecular phenotypes may provide new areas of investigation for ATM function or may be exploited by designing specific therapies for MCL cases with p53 aberrations...
  88. ncbi request reprint Identification of a proliferation signature related to survival in nodal peripheral T-cell lymphomas
    Marta Cuadros
    Human Genetics Group and Genotyping Unit, Human Cancer Genetics Program, Spanish National Cancer Centre, Madrid, Spain
    J Clin Oncol 25:3321-9. 2007
    ..Initial expression profiling studies of T-cell lymphomas have been inconclusive in yielding clinically relevant insights. We applied DNA microarrays to gain insight into the molecular signatures associated with prognosis. Materials and..
  89. pmc Repression of BCL-6 is required for the formation of human memory B cells in vitro
    Tracy C Kuo
    Department of Microbiology, Columbia University Medical Center, New York, NY 10032, USA
    J Exp Med 204:819-30. 2007
    ..These studies establish new molecular criteria for defining the memory B cell stage in human B cells...
  90. pmc Specific secondary genetic alterations in mantle cell lymphoma provide prognostic information independent of the gene expression-based proliferation signature
    Itziar Salaverria
    Department of Pathology and Hematology, Hospital Clinic, University of Barcelona, Barcelona, Spain
    J Clin Oncol 25:1216-22. 2007
    ....
  91. pmc Transformation of follicular lymphoma to diffuse large B-cell lymphoma proceeds by distinct oncogenic mechanisms
    Andrew J Davies
    Cancer Research UK Medical Oncology Unit, St Bartholomew s Hospital, London, UK
    Br J Haematol 136:286-93. 2007
    ....
  92. ncbi request reprint C-myc activation impairs the NF-kappaB and the interferon response: implications for the pathogenesis of Burkitt's lymphoma
    Martin Schlee
    Institute of Clinical Molecular Biology and Tumor Genetics, GSF National Research Center for Environment and Health, Munchen, Germany
    Int J Cancer 120:1387-95. 2007
    ..c-MYC thus masks an interferon-inducing activity in these cells. Our findings imply that immune escape of tumor cells is not only a matter of in vivo selection but may be additionally promoted by activation of a cellular oncogene...
  93. ncbi request reprint BCL-6 and rituximab in diffuse large B-cell lymphoma: where are we?
    Kieron Dunleavy
    Blood 109:843-4; discussion 844-5. 2007
  94. ncbi request reprint Homozygous deletions localize novel tumor suppressor genes in B-cell lymphomas
    Cinta Mestre-Escorihuela
    Center for Applied Medical Research CIMA, University of Navarra, Avda Pio XII, 55, Pamplona 31008, Spain
    Blood 109:271-80. 2007
    ..Our microarray strategy has identified novel candidate tumor suppressor genes inactivated by genetic and epigenetic mechanisms that substantially vary among the B-NHL subtypes...
  95. ncbi request reprint Graded expression of interferon regulatory factor-4 coordinates isotype switching with plasma cell differentiation
    Roger Sciammas
    Howard Hughes Medical Institute, Department of Molecular Genetics and Cell Biology, The University of Chicago, Chicago, Illinois 60637, USA
    Immunity 25:225-36. 2006
    ..We propose a gene-regulatory network in which graded expression of IRF-4 developmentally coordinates isotype switching with plasma cell differentiation...
  96. pmc Diffuse large B-cell lymphoma subgroups have distinct genetic profiles that influence tumor biology and improve gene-expression-based survival prediction
    Silvia Bea
    Department of Pathology and Hematology Hospital Clinic, University of Barcelona, Spain
    Blood 106:3183-90. 2005
    ..In addition, gains involving the chromosomal region 3p11-p12 provided prognostic information that was statistically independent of the previously defined gene-expression-based survival model, thereby improving its predictive power...
  97. pmc Loss of major histocompatibility class II gene and protein expression in primary mediastinal large B-cell lymphoma is highly coordinated and related to poor patient survival
    Robin A Roberts
    Department of Pathology, University of Arizona, Tucson, AZ 85724 5043, USA
    Blood 108:311-8. 2006
    ..Although overall survival was better, survival of the lowest 10% of MHC II expressers was similarly poor in DLBCL and PMBCL. MHC II expression may define a therapeutic target in both these diseases...
  98. pmc Stereotyped and specific gene expression programs in human innate immune responses to bacteria
    Jennifer C Boldrick
    Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, CA 94305, USA
    Proc Natl Acad Sci U S A 99:972-7. 2002
    ..Modulation of this host-response program by bacterial virulence mechanisms was an important source of variation in the response to different bacteria...