The genetic landscape of diffuse large B-cell lymphoma.
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[1] S. Swerdlow. WHO Classification of Tumours of Haematopoietic and Lymphoid Tissues , 2017 .
[2] Adrien B. Larsen,et al. Loss of signaling via Gα13 in germinal center B cell-derived lymphoma , 2014, Nature.
[3] Raul Rabadan,et al. Genetics of follicular lymphoma transformation. , 2014, Cell reports.
[4] L. Ferrarini,et al. Germinal center dysregulation by histone methyltransferase EZH2 promotes lymphomagenesis. , 2013, The Journal of clinical investigation.
[5] K. Basso,et al. MEF2B mutations lead to deregulated expression of the BCL6 oncogene in Diffuse Large B cell Lymphoma , 2013, Nature Immunology.
[6] David I Heiman,et al. Mutational heterogeneity in cancer and the search for new cancer genes , 2013, Nature.
[7] O. Elemento,et al. EZH2 is required for germinal center formation and somatic EZH2 mutations promote lymphoid transformation. , 2013, Cancer cell.
[8] Steven J. M. Jones,et al. Analysis of FOXO1 mutations in diffuse large B-cell lymphoma. , 2013, Blood.
[9] Ash A. Alizadeh,et al. Hierarchy in somatic mutations arising during genomic evolution and progression of follicular lymphoma. , 2012, Blood.
[10] Steven J. M. Jones,et al. Recurrent targets of aberrant somatic hypermutation in lymphoma , 2012, Oncotarget.
[11] K. Rajewsky,et al. MYC is essential for the formation and maintenance of germinal centers , 2012, Nature Immunology.
[12] M. Nussenzweig,et al. The proto-oncogene MYC is required for selection in the germinal center and cyclic reentry , 2012, Nature Immunology.
[13] M. Nussenzweig,et al. Identification of human germinal center light and dark zone cells and their relationship to human B-cell lymphomas. , 2012, Blood.
[14] Stefano Monti,et al. Integrative analysis reveals an outcome-associated and targetable pattern of p53 and cell cycle deregulation in diffuse large B cell lymphoma. , 2012, Cancer cell.
[15] K. Basso,et al. Roles of BCL6 in normal and transformed germinal center B cells , 2012, Immunological reviews.
[16] Eric S. Lander,et al. Discovery and prioritization of somatic mutations in diffuse large B-cell lymphoma (DLBCL) by whole-exome sequencing , 2012, Proceedings of the National Academy of Sciences.
[17] Michele Pagano,et al. FBXO11 targets BCL6 for degradation and is inactivated in diffuse large B-cell lymphomas , 2012, Nature.
[18] Govind Bhagat,et al. Combined genetic inactivation of β2-Microglobulin and CD58 reveals frequent escape from immune recognition in diffuse large B cell lymphoma. , 2011, Cancer cell.
[19] Christian Steidl,et al. The molecular pathogenesis of primary mediastinal large B-cell lymphoma. , 2011, Blood.
[20] Steven J. M. Jones,et al. Frequent mutation of histone modifying genes in non-Hodgkin lymphoma , 2011, Nature.
[21] Raul Rabadan,et al. Analysis of the Coding Genome of Diffuse Large B-Cell Lymphoma , 2011, Nature Genetics.
[22] Ryan D. Morin,et al. Somatic mutations at EZH2 Y641 act dominantly through a mechanism of selectively altered PRC2 catalytic activity, to increase H3K27 trimethylation. , 2011, Blood.
[23] Joseph M. Connors,et al. Oncogenically active MYD88 mutations in human lymphoma , 2011, Nature.
[24] Raul Rabadan,et al. Inactivating mutations of acetyltransferase genes in B-cell lymphoma , 2010, Nature.
[25] J. Kutok,et al. Constitutive canonical NF-κB activation cooperates with disruption of BLIMP1 in the pathogenesis of activated B cell-like diffuse large cell lymphoma. , 2010, Cancer cell.
[26] L. Pasqualucci,et al. BLIMP1 is a tumor suppressor gene frequently disrupted in activated B cell-like diffuse large B cell lymphoma. , 2010, Cancer cell.
[27] Jan Delabie,et al. Chronic active B-cell-receptor signalling in diffuse large B-cell lymphoma , 2010, Nature.
[28] Ryan D. Morin,et al. Somatic mutation of EZH2 (Y641) in Follicular and Diffuse Large B-cell Lymphomas of Germinal Center Origin , 2010, Nature Genetics.
[29] K. Basso,et al. BCL6 suppression of BCL2 via Miz1 and its disruption in diffuse large B cell lymphoma , 2009, Proceedings of the National Academy of Sciences.
[30] L. Pasqualucci,et al. Mutations of multiple genes cause deregulation of NF-κB in diffuse large B-cell lymphoma , 2009, Nature.
[31] S. Ogawa,et al. Frequent inactivation of A20 in B-cell lymphomas , 2009, Nature.
[32] L. Staudt,et al. Molecular subtypes of diffuse large B-cell lymphoma arise by distinct genetic pathways , 2008, Proceedings of the National Academy of Sciences.
[33] Jan Delabie,et al. Oncogenic CARD11 Mutations in Human Diffuse Large B Cell Lymphoma , 2008, Science.
[34] D. Schatz,et al. Two levels of protection for the B cell genome during somatic hypermutation , 2008, Nature.
[35] L. Staudt,et al. Distinctive patterns of BCL6 molecular alterations and their functional consequences in different subgroups of diffuse large B-cell lymphoma , 2007, Leukemia.
[36] M. Shipp,et al. BCL6 programs lymphoma cells for survival and differentiation through distinct biochemical mechanisms. , 2007, Blood.
[37] K. Basso,et al. A signaling pathway mediating downregulation of BCL6 in germinal center B cells is blocked by BCL6 gene alterations in B cell lymphoma. , 2007, Cancer cell.
[38] L. Staudt,et al. Aberrant immunoglobulin class switch recombination and switch translocations in activated B cell–like diffuse large B cell lymphoma , 2007, The Journal of experimental medicine.
[39] W. Chan,et al. Mutational analysis of PRDM1 indicates a tumor-suppressor role in diffuse large B-cell lymphomas. , 2006, Blood.
[40] Stefano Monti,et al. Inactivation of the PRDM1/BLIMP1 gene in diffuse large B cell lymphoma , 2006, The Journal of experimental medicine.
[41] Peter Cresswell,et al. Mechanisms of MHC class I‐restricted antigen processing and cross‐presentation , 2005, Immunological reviews.
[42] Qiong Shen,et al. Deregulated BCL6 expression recapitulates the pathogenesis of human diffuse large B cell lymphomas in mice. , 2005, Cancer cell.
[43] Ryan T. Phan,et al. The BCL6 proto-oncogene suppresses p53 expression in germinal-centre B cells , 2004, Nature.
[44] T. Golub,et al. Molecular profiling of diffuse large B-cell lymphoma identifies robust subtypes including one characterized by host inflammatory response. , 2004, Blood.
[45] Matthew T Wheeler,et al. The ubiquitin-modifying enzyme A20 is required for termination of Toll-like receptor responses , 2004, Nature Immunology.
[46] M. Nussenzweig,et al. AID Is Required for c-myc/IgH Chromosome Translocations In Vivo , 2004, Cell.
[47] M. Thome. CARMA1, BCL-10 and MALT1 in lymphocyte development and activation , 2004, Nature Reviews Immunology.
[48] 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.
[49] K. Calame,et al. Blimp-1 is required for the formation of immunoglobulin secreting plasma cells and pre-plasma memory B cells. , 2003, Immunity.
[50] 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.
[51] Katia Basso,et al. Mutations of the BCL6 proto-oncogene disrupt its negative autoregulation in diffuse large B-cell lymphoma. , 2003, Blood.
[52] A. Naganuma,et al. Negative autoregulation of BCL-6 is bypassed by genetic alterations in diffuse large B cell lymphomas , 2002, Proceedings of the National Academy of Sciences of the United States of America.
[53] Wei Gu,et al. Acetylation inactivates the transcriptional repressor BCL6 , 2002, Nature Genetics.
[54] Meland,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.
[55] 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.
[56] Riccardo Dalla-Favera,et al. Mechanisms of chromosomal translocations in B cell lymphomas , 2001, Oncogene.
[57] Gouri Nanjangud,et al. Hypermutation of multiple proto-oncogenes in B-cell diffuse large-cell lymphomas , 2001, Nature.
[58] T. Honjo,et al. Class Switch Recombination and Hypermutation Require Activation-Induced Cytidine Deaminase (AID), a Potential RNA Editing Enzyme , 2000, Cell.
[59] A. Fischer,et al. Activation-Induced Cytidine Deaminase (AID) Deficiency Causes the Autosomal Recessive Form of the Hyper-IgM Syndrome (HIGM2) , 2000, Cell.
[60] 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.
[61] R. Goodman,et al. CBP/p300 in cell growth, transformation, and development. , 2000, Genes & development.
[62] Ash A. Alizadeh,et al. Distinct types of diffuse large B-cell lymphoma identified by gene expression profiling , 2000, Nature.
[63] L. Pasqualucci,et al. BCL-6 mutations in normal germinal center B cells: evidence of somatic hypermutation acting outside Ig loci. , 1998, Proceedings of the National Academy of Sciences of the United States of America.
[64] U. Storb,et al. Mutation of BCL-6 gene in normal B cells by the process of somatic hypermutation of Ig genes. , 1998, Science.
[65] K Offit,et al. Alterations of a zinc finger-encoding gene, BCL-6, in diffuse large-cell lymphoma. , 1993, Science.
[66] L. Staudt,et al. Diffuse large B-cell lymphoma—treatment approaches in the molecular era , 2014, Nature Reviews Clinical Oncology.
[67] M. Nussenzweig,et al. Deep-sequencing identification of the genomic targets of the cytidine deaminase AID and its cofactor RPA in B lymphocytes , 2011, Nature Immunology.
[68] Riccardo Dalla-Favera,et al. Germinal centres: role in B-cell physiology and malignancy , 2008, Nature Reviews Immunology.
[69] L. Pasqualucci,et al. AID is required for germinal center–derived lymphomagenesis , 2008, Nature Genetics.
[70] L. Staudt,et al. Confirmation of the molecular classification of diffuse large B-cell lymphoma by immunohistochemistry using a tissue microarray. , 2004, Blood.