Integrating genomic alterations in diffuse large B-cell lymphoma identifies new relevant pathways and potential therapeutic targets

[1]  C. Popp,et al.  Tumor Microenvironment in Diffuse Large B-Cell Lymphoma: Role and Prognosis , 2019, Analytical cellular pathology.

[2]  M. Katoh,et al.  Precision medicine for human cancers with Notch signaling dysregulation (Review) , 2019, International journal of molecular medicine.

[3]  W. Wilson,et al.  The landscape of new drugs in lymphoma , 2017, Nature Reviews Clinical Oncology.

[4]  C. Mamot,et al.  Mutations of CREBBP and SOCS1 are independent prognostic factors in diffuse large B cell lymphoma: mutational analysis of the SAKK 38/07 prospective clinical trial cohort , 2017, Journal of Hematology & Oncology.

[5]  Christopher A. Miller,et al.  Recurrent somatic mutations affecting B-cell receptor signaling pathway genes in follicular lymphoma. , 2017, Blood.

[6]  Shaoping Ling,et al.  Mutations or copy number losses of CD58 and TP53 genes in diffuse large B cell lymphoma are independent unfavorable prognostic factors , 2016, Oncotarget.

[7]  L. Staudt,et al.  Epigenetic gene regulation by Janus kinase 1 in diffuse large B-cell lymphoma , 2016, Proceedings of the National Academy of Sciences.

[8]  L. Pasqualucci,et al.  Loss of PRDM1/BLIMP-1 function contributes to poor prognosis of activated B-cell-like diffuse large B-cell lymphoma , 2016, Leukemia.

[9]  C. Ruiz,et al.  Distinct genetic evolution patterns of relapsing diffuse large B-cell lymphoma revealed by genome-wide copy number aberration and targeted sequencing analysis , 2016, Leukemia.

[10]  C. Copie-Bergman,et al.  Next-Generation Sequencing in Diffuse Large B-Cell Lymphoma Highlights Molecular Divergence and Therapeutic Opportunities: a LYSA Study , 2016, Clinical Cancer Research.

[11]  M. Kersten,et al.  Precision medicine in diffuse large B-cell lymphoma: hitting the target , 2015, Haematologica.

[12]  Michael T. Zimmermann,et al.  Whole-exome analysis reveals novel somatic genomic alterations associated with outcome in immunochemotherapy-treated diffuse large B-cell lymphoma , 2015, Blood Cancer Journal.

[13]  A. Valencia,et al.  Non-coding recurrent mutations in chronic lymphocytic leukaemia , 2015, Nature.

[14]  R. Verhaak,et al.  Seek and destroy: relating cancer drivers to therapies. , 2015, Cancer cell.

[15]  Michael P. Schroeder,et al.  In silico prescription of anticancer drugs to cohorts of 28 tumor types reveals targeting opportunities. , 2015, Cancer cell.

[16]  W. Klapper,et al.  Characterization of genomic imbalances in diffuse large B‐cell lymphoma by detailed SNP‐chip analysis , 2015, International journal of cancer.

[17]  Ryan D. Morin,et al.  An RCOR1 loss-associated gene expression signature identifies a prognostically significant DLBCL subgroup. , 2015, Blood.

[18]  S. Friend,et al.  Database of genomic biomarkers for cancer drugs and clinical targetability in solid tumors. , 2015, Cancer discovery.

[19]  E. Giné,et al.  Recurrent mutations of NOTCH genes in follicular lymphoma identify a distinctive subset of tumours , 2014, The Journal of pathology.

[20]  A. Intlekofer,et al.  Precision therapy for lymphoma—current state and future directions , 2014, Nature Reviews Clinical Oncology.

[21]  Bruce D Cheson,et al.  Recommendations for initial evaluation, staging, and response assessment of Hodgkin and non-Hodgkin lymphoma: the Lugano classification. , 2014, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.

[22]  Kai Fu,et al.  Determining cell-of-origin subtypes of diffuse large B-cell lymphoma using gene expression in formalin-fixed paraffin-embedded tissue. , 2014, Blood.

[23]  F. Jardin,et al.  Targetable activating mutations are very frequent in GCB and ABC diffuse large B‐cell lymphoma , 2014, Genes, chromosomes & cancer.

[24]  M. Calaminici,et al.  Integrated genomic analysis identifies recurrent mutations and evolution patterns driving the initiation and progression of follicular lymphoma , 2013, Nature Genetics.

[25]  Manel Juan,et al.  Landscape of somatic mutations and clonal evolution in mantle cell lymphoma , 2013, Proceedings of the National Academy of Sciences.

[26]  David Tamborero,et al.  OncodriveCLUST: exploiting the positional clustering of somatic mutations to identify cancer genes , 2013, Bioinform..

[27]  Steven J. M. Jones,et al.  Mutational and structural analysis of diffuse large B-cell lymphoma using whole-genome sequencing. , 2013, Blood.

[28]  F. Jardin,et al.  The costimulatory molecule CD70 is regulated by distinct molecular mechanisms and is associated with overall survival in diffuse large B‐cell lymphoma , 2013, Genes, chromosomes & cancer.

[29]  G. Lenz,et al.  PTEN loss defines a PI3K/AKT pathway-dependent germinal center subtype of diffuse large B-cell lymphoma , 2013, Proceedings of the National Academy of Sciences.

[30]  T. Haferlach,et al.  STAT3 mutations are highly specific for large granular lymphocytic leukemia , 2013, Leukemia.

[31]  Steven J. M. Jones,et al.  Analysis of FOXO1 mutations in diffuse large B-cell lymphoma. , 2013, Blood.

[32]  David Dunson,et al.  Genetic heterogeneity of diffuse large B-cell lymphoma , 2013, Proceedings of the National Academy of Sciences.

[33]  R. Spang,et al.  SOCS1 Mutation Subtypes Predict Divergent Outcomes in Diffuse Large B-Cell Lymphoma (DLBCL) Patients , 2012, Oncotarget.

[34]  R. Spang,et al.  Recurrent mutation of the ID3 gene in Burkitt lymphoma identified by integrated genome, exome and transcriptome sequencing , 2012, Nature Genetics.

[35]  Dereje D. Jima,et al.  The genetic landscape of mutations in Burkitt lymphoma , 2012, Nature Genetics.

[36]  W. Choi,et al.  Mutational profile and prognostic significance of TP53 in diffuse large B-cell lymphoma patients treated with R-CHOP: report from an International DLBCL Rituximab-CHOP Consortium Program Study. , 2012, Blood.

[37]  Steven J. M. Jones,et al.  Recurrent targets of aberrant somatic hypermutation in lymphoma , 2012, Oncotarget.

[38]  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.

[39]  K. Cibulskis,et al.  Integrative genome analyses identify key somatic driver mutations of small-cell lung cancer , 2012, Nature Genetics.

[40]  K. Elenitoba-Johnson,et al.  Whole-genome sequencing identifies recurrent somatic NOTCH2 mutations in splenic marginal zone lymphoma , 2012, The Journal of experimental medicine.

[41]  S. Pileri,et al.  The coding genome of splenic marginal zone lymphoma: activation of NOTCH2 and other pathways regulating marginal zone development , 2012, The Journal of experimental medicine.

[42]  K. Hoang-Xuan,et al.  Recurrent Mutations of MYD88 and TBL1XR1 in Primary Central Nervous System Lymphomas , 2012, Clinical Cancer Research.

[43]  Ryan D. Morin,et al.  BCL2 mutations in diffuse large B-cell lymphoma , 2012, Leukemia.

[44]  F. Lang,et al.  Phosphorylation of Nicastrin by SGK1 Leads to Its Degradation through Lysosomal and Proteasomal Pathways , 2012, PloS one.

[45]  Paul K. Brindle,et al.  Is histone acetylation the most important physiological function for CBP and p300? , 2012, Aging.

[46]  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.

[47]  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.

[48]  Steven J. M. Jones,et al.  Frequent mutation of histone modifying genes in non-Hodgkin lymphoma , 2011, Nature.

[49]  Raul Rabadan,et al.  Analysis of the Coding Genome of Diffuse Large B-Cell Lymphoma , 2011, Nature Genetics.

[50]  Juliane C. Dohm,et al.  Whole-genome sequencing identifies recurrent mutations in chronic lymphocytic leukaemia , 2011, Nature.

[51]  C. Sander,et al.  Predicting the functional impact of protein mutations: application to cancer genomics , 2011, Nucleic acids research.

[52]  J. Sprent,et al.  ATP11C is critical for the internalization of phosphatidylserine and differentiation of B lymphocytes , 2011, Nature Immunology.

[53]  A. Gonzalez-Perez,et al.  Improving the assessment of the outcome of nonsynonymous SNVs with a consensus deleteriousness score, Condel. , 2011, American journal of human genetics.

[54]  Kenneth H. Buetow,et al.  CREBBP mutations in relapsed acute lymphoblastic leukaemia , 2011, Nature.

[55]  B. Beutler,et al.  The P4-type ATPase ATP11C is essential for B lymphopoiesis in adult bone marrow , 2011, Nature Immunology.

[56]  Joseph M. Connors,et al.  Oncogenically active MYD88 mutations in human lymphoma , 2011, Nature.

[57]  F. Lang,et al.  Serum- and glucocorticoid-inducible kinase 1 (SGK1) controls Notch1 signaling by downregulation of protein stability through Fbw7 ubiquitin ligase , 2011, Journal of Cell Science.

[58]  Raul Rabadan,et al.  Inactivating mutations of acetyltransferase genes in B-cell lymphoma , 2010, Nature.

[59]  Govind Bhagat,et al.  BLIMP1 is a tumor suppressor gene frequently disrupted in activated B cell-like diffuse large B cell lymphoma. , 2010, Cancer cell.

[60]  W. Chan,et al.  Genomic lesions associated with a different clinical outcome in diffuse large B‐Cell lymphoma treated with R‐CHOP‐21 , 2010, British journal of haematology.

[61]  T. Molina,et al.  Diffuse large B-cell lymphomas with CDKN2A deletion have a distinct gene expression signature and a poor prognosis under R-CHOP treatment: a GELA study. , 2010, Blood.

[62]  Jana Marie Schwarz,et al.  MutationTaster evaluates disease-causing potential of sequence alterations , 2010, Nature Methods.

[63]  P. Bork,et al.  A method and server for predicting damaging missense mutations , 2010, Nature Methods.

[64]  J. Soulier,et al.  Mutation in TET2 in myeloid cancers. , 2009, The New England journal of medicine.

[65]  A. Mottok,et al.  Inactivating SOCS1 mutations are caused by aberrant somatic hypermutation and restricted to a subset of B-cell lymphoma entities. , 2009, Blood.

[66]  H. Tagawa,et al.  TNFAIP3/A20 functions as a novel tumor suppressor gene in several subtypes of non-Hodgkin lymphomas. , 2009, Blood.

[67]  Leyla Isik,et al.  Cancer-specific high-throughput annotation of somatic mutations: computational prediction of driver missense mutations. , 2009, Cancer research.

[68]  K. Owzar,et al.  Correlation of kinase genotype and clinical outcome in the North American Intergroup Phase III Trial of imatinib mesylate for treatment of advanced gastrointestinal stromal tumor: CALGB 150105 Study by Cancer and Leukemia Group B and Southwest Oncology Group. , 2008, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.

[69]  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.

[70]  L. Staudt,et al.  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. , 2008, Blood.

[71]  T. Golub,et al.  Integrative analysis reveals 53BP1 copy loss and decreased expression in a subset of human diffuse large B-cell lymphomas , 2008, Oncogene.

[72]  G. Cattoretti,et al.  Constitutively activated STAT3 promotes cell proliferation and survival in the activated B-cell subtype of diffuse large B-cell lymphomas. , 2007, Blood.

[73]  A. Look,et al.  Mechanisms of transcription factor deregulation in lymphoid cell transformation , 2007, Oncogene.

[74]  B. Coiffier Rituximab therapy in malignant lymphoma , 2007, Oncogene.

[75]  M. Bhasin,et al.  Notch1 Contributes to Mouse T-Cell Leukemia by Directly Inducing the Expression of c-myc , 2006, Molecular and Cellular Biology.

[76]  J. Aster,et al.  c-Myc is an important direct target of Notch1 in T-cell acute lymphoblastic leukemia/lymphoma. , 2006, Genes & development.

[77]  Stefano Monti,et al.  Inactivation of the PRDM1/BLIMP1 gene in diffuse large B cell lymphoma , 2006, The Journal of experimental medicine.

[78]  L. Staudt,et al.  Diffuse large B-cell lymphoma subgroups have distinct genetic profiles that influence tumor biology and improve gene-expression-based survival prediction. , 2005, Blood.

[79]  H. Tagawa,et al.  Comparison of genome profiles for identification of distinct subgroups of diffuse large B-cell lymphoma. , 2005, Blood.

[80]  Katia Basso,et al.  Mutations of the BCL6 proto-oncogene disrupt its negative autoregulation in diffuse large B-cell lymphoma. , 2003, Blood.

[81]  A. Nicholson,et al.  Mutations of the BRAF gene in human cancer , 2002, Nature.

[82]  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.

[83]  D. Hossfeld E.S. Jaffe, N.L. Harris, H. Stein, J.W. Vardiman (eds). World Health Organization Classification of Tumours: Pathology and Genetics of Tumours of Haematopoietic and Lymphoid Tissues , 2002 .

[84]  Gouri Nanjangud,et al.  Hypermutation of multiple proto-oncogenes in B-cell diffuse large-cell lymphomas , 2001, Nature.

[85]  Ash A. Alizadeh,et al.  Distinct types of diffuse large B-cell lymphoma identified by gene expression profiling , 2000, Nature.

[86]  E. Campo,et al.  p16(INK4a) gene inactivation by deletions, mutations, and hypermethylation is associated with transformed and aggressive variants of non-Hodgkin's lymphomas. , 1998, Blood.

[87]  Steven A. Roberts,et al.  Mutational heterogeneity in cancer and the search for new cancer genes , 2014 .

[88]  Ryan D. Morin,et al.  Whole transcriptome sequencing reveals recurrent NOTCH1 mutations in mantle cell lymphoma. , 2012, Blood.

[89]  S. Henikoff,et al.  Predicting the effects of coding non-synonymous variants on protein function using the SIFT algorithm , 2009, Nature Protocols.

[90]  L. Staudt,et al.  Confirmation of the molecular classification of diffuse large B-cell lymphoma by immunohistochemistry using a tissue microarray. , 2004, Blood.

[91]  Emili Montserrat,et al.  Clinical impact of the differentiation profile assessed by immunophenotyping in patients with diffuse large B-cell lymphoma. , 2003, Blood.

[92]  E. Campo,et al.  p16(INK4a) gene inactivation by deletions, mutations, and hypermethylation is associated with transformed and aggressive variants of non-Hodgkin's lymphomas. , 1998, Blood.