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langid = {english}

}

title = {Enhancing Knowledge Discovery from Cancer Genomics Data with {{Galaxy}}},

author = {Albuquerque, Marco A. and Grande, Bruno M. and Ritch, Elie J. and Pararajalingam, Prasath and Jessa, Selin and Krzywinski, Martin and Grewal, Jasleen K. and Shah, Sohrab P. and Boutros, Paul C. and Morin, Ryan D.},

date = {2017-05-01},

abstract = {Rituximab, a type I anti-CD20 monoclonal antibody (mAb), induces incomplete B cell depletion in some patients with rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE), thus contributing to a poor clinical response. The mechanisms of this resistance remain elusive. The purpose of this study was to determine whether type II mAb are more efficient than type I mAb at depleting B cells from RA and SLE patients, whether internalization influences the efficiency of depletion, and whether Fcγ receptor type IIb (FcγRIIb) and the B cell receptor regulate this internalization process. We used an in vitro whole blood B cell–depletion assay to assess the efficiency of depletion, flow cytometry to study cell surface protein expression, and surface fluorescence–quenching assays to assess rituximab internalization, in samples from patients with RA and patients with SLE. Paired t-test or Mann-Whitney U test was used to compare groups, and Spearman's rank correlation test was used to assess correlation. We found that type II mAb internalized significantly less rituximab than type I mAb and depleted B cells from patients with RA and SLE at least 2-fold more efficiently than type I mAb. Internalization of rituximab was highly variable between patients, was regulated by FcγRIIb, and inversely correlated with cytotoxicity in whole blood B cell–depletion assays. The lowest levels of internalization were seen in IgD– B cells, including postswitched (IgD–CD27+) memory cells. Internalization of type I anti-CD20 mAb was also partially inhibited by anti-IgM stimulation. Variability in internalization of rituximab was observed and was correlated with impaired B cell depletion. Therefore, slower-internalizing type II mAb should be considered as alternative B cell–depleting agents for the treatment of RA and SLE.}

}

title = {Flow Sorting and Exome Sequencing Reveal the Oncogenome of Primary {{Hodgkin}} and {{Reed-Sternberg}} Cells},

author = {Reichel, Jonathan and Chadburn, Amy and Rubinstein, Paul G. and Giulino-Roth, Lisa and Tam, Wayne and Liu, Yifang and Gaiolla, Rafael and Eng, Kenneth and Brody, Joshua and Inghirami, Giorgio and Carlo-Stella, Carmelo and Santoro, Armando and Rahal, Daoud and Totonchy, Jennifer and Elemento, Olivier and Cesarman, Ethel and Roshal, Mikhail},

date = {2015-02-12},

keywords = {Antineoplastic Combined Chemotherapy Protocols,Biopsy,Epigenesis Genetic,Exome,Gene Expression Profiling,Genetic Heterogeneity,Genotype,Humans,Kaplan-Meier Estimate,Lymphoma Large B-Cell Diffuse,Mutation,Prognosis,Sequence Analysis DNA,Transcriptome}

}

title = {{{TNFAIP3}} ({{A20}}) Is a Tumor Suppressor Gene in {{Hodgkin}} Lymphoma and Primary Mediastinal {{B}} Cell Lymphoma},

author = {Schmitz, Roland and Hansmann, Martin-Leo and Bohle, Verena and Martin-Subero, Jose Ignacio and Hartmann, Sylvia and Mechtersheimer, Gunhild and Klapper, Wolfram and Vater, Inga and Giefing, Maciej and Gesk, Stefan and Stanelle, Jens and Siebert, Reiner and Küppers, Ralf},

date = {2009-05-11},

keywords = {Cell Line Tumor,Chromosome Deletion,DNA Transposable Elements,DNA-Binding Proteins,Epstein-Barr Virus Infections,Frameshift Mutation,Genes Tumor Suppressor,Hodgkin Disease,Humans,Intracellular Signaling Peptides and Proteins,Lymphoma B-Cell,Mutation,Mutation Missense,Nuclear Proteins,Polymorphism Single Nucleotide,Transcription Genetic,Tumor Necrosis Factor alpha-Induced Protein 3}

}

title = {Alterations of the {{CD58}} Gene in Classical {{Hodgkin}} Lymphoma},

author = {Schneider, Markus and Schneider, Stefanie and Zühlke-Jenisch, Reina and Klapper, Wolfram and Sundström, Christer and Hartmann, Sylvia and Hansmann, Martin-Leo and Siebert, Reiner and Küppers, Ralf and Giefing, Maciej},

date = {2015-10},