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  • Articles  (5)
  • 2005-2009  (5)
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  • 1
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    Broad diversity of neutralizing antibodies isolated from memory B cells in HIV-infected individuals (2009)
    Nature Publishing Group (NPG)
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    Publication Date: 2009-03-17
    Description: Antibodies to conserved epitopes on the human immunodeficiency virus (HIV) surface protein gp140 can protect against infection in non-human primates, and some infected individuals show high titres of broadly neutralizing immunoglobulin (Ig)G antibodies in their serum. However, little is known about the specificity and activity of these antibodies. To characterize the memory antibody responses to HIV, we cloned 502 antibodies from HIV envelope-binding memory B cells from six HIV-infected patients with broadly neutralizing antibodies and low to intermediate viral loads. We show that in these patients, the B-cell memory response to gp140 is composed of up to 50 independent clones expressing high affinity neutralizing antibodies to the gp120 variable loops, the CD4-binding site, the co-receptor-binding site, and to a new neutralizing epitope that is in the same region of gp120 as the CD4-binding site. Thus, the IgG memory B-cell compartment in the selected group of patients with broad serum neutralizing activity to HIV is comprised of multiple clonal responses with neutralizing activity directed against several epitopes on gp120.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Scheid, Johannes F -- Mouquet, Hugo -- Feldhahn, Niklas -- Seaman, Michael S -- Velinzon, Klara -- Pietzsch, John -- Ott, Rene G -- Anthony, Robert M -- Zebroski, Henry -- Hurley, Arlene -- Phogat, Adhuna -- Chakrabarti, Bimal -- Li, Yuxing -- Connors, Mark -- Pereyra, Florencia -- Walker, Bruce D -- Wardemann, Hedda -- Ho, David -- Wyatt, Richard T -- Mascola, John R -- Ravetch, Jeffrey V -- Nussenzweig, Michel C -- Howard Hughes Medical Institute/ -- Intramural NIH HHS/ -- England -- Nature. 2009 Apr 2;458(7238):636-40. doi: 10.1038/nature07930. Epub 2009 Mar 15.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular Immunology, The Rockefeller University, New York, New York 10065, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19287373" target="_blank"〉PubMed〈/a〉
    Keywords: Antibody Affinity ; Antigens, CD4/metabolism ; B-Lymphocytes/*immunology ; Binding Sites ; Enzyme-Linked Immunosorbent Assay ; Epitope Mapping ; Epitopes, B-Lymphocyte/chemistry/immunology ; HIV Antibodies/*analysis/*immunology/isolation & purification ; HIV Envelope Protein gp120/chemistry/immunology/metabolism ; HIV Envelope Protein gp41/chemistry/immunology ; HIV Infections/*immunology ; Humans ; Immunologic Memory/*immunology ; Neutralization Tests ; Receptors, HIV/metabolism ; Viral Load ; env Gene Products, Human Immunodeficiency Virus/chemistry/*immunology/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 2
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    Oncogenic CARD11 mutations in human diffuse large B cell lymphoma (2008)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2008-03-08
    Description: Diffuse large B cell lymphoma (DLBCL) is the most common form of non-Hodgkin's lymphoma. In the least curable (ABC) subtype of DLBCL, survival of the malignant cells is dependent on constitutive activation of the nuclear factor-kappaB (NF-kappaB) signaling pathway. In normal B cells, antigen receptor-induced NF-kappaB activation requires CARD11, a cytoplasmic scaffolding protein. To determine whether CARD11 contributes to tumorigenesis, we sequenced the CARD11 gene in human DLBCL tumors. We detected missense mutations in 7 of 73 ABC DLBCL biopsies (9.6%), all within exons encoding the coiled-coil domain. Experimental introduction of CARD11 coiled-coil domain mutants into lymphoma cell lines resulted in constitutive NF-kappaB activation and enhanced NF-kappaB activity upon antigen receptor stimulation. 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.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lenz, Georg -- Davis, R Eric -- Ngo, Vu N -- Lam, Lloyd -- George, Thaddeus C -- Wright, George W -- Dave, Sandeep S -- Zhao, Hong -- Xu, Weihong -- Rosenwald, Andreas -- Ott, German -- Muller-Hermelink, Hans Konrad -- Gascoyne, Randy D -- Connors, Joseph M -- Rimsza, Lisa M -- Campo, Elias -- Jaffe, Elaine S -- Delabie, Jan -- Smeland, Erlend B -- Fisher, Richard I -- Chan, Wing C -- Staudt, Louis M -- UO1-CA84967/CA/NCI NIH HHS/ -- Intramural NIH HHS/ -- New York, N.Y. -- Science. 2008 Mar 21;319(5870):1676-9. doi: 10.1126/science.1153629. Epub 2008 Mar 6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Metabolism Branch, Division of Cancer Treatment and Diagnosis, Center for Cancer Research, National Cancer Institute, Bethesda, MD 20892, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18323416" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Apoptosis Regulatory Proteins/chemistry/*genetics/metabolism ; CARD Signaling Adaptor Proteins/chemistry/*genetics/metabolism ; Cell Line, Tumor ; Cytoplasm/metabolism ; Guanylate Cyclase/chemistry/*genetics/metabolism ; Humans ; I-kappa B Kinase/metabolism ; Jurkat Cells ; Lymphoma, Large B-Cell, Diffuse/*genetics ; Molecular Sequence Data ; *Mutation, Missense ; NF-kappa B ; *Oncogenes ; Protein Structure, Tertiary ; Receptors, Antigen, B-Cell/physiology ; Sequence Analysis, DNA
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 3
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    Molecular subtypes of diffuse large B-cell lymphoma arise by distinct genetic pathways (2008)
    National Academy of Sciences
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    Publication Date: 2008-09-02
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Published by National Academy of Sciences
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  • 4
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    Distinctive Patterns of BCL6 Molecular Alterations in Different Subsets of Diffuse Large B-Cell Lymphoma and Their Functional Consequences. (2005)
    American Society of Hematology
    Details
    Publication Date: 2005-11-16
    Description: Gene expression profiling of diffuse large B-cell lymphoma (DLBCL) has revealed biologically and prognostically distinct subgroups: germinal center B-cell-like (GCB), activated B cell-like (ABC), and primary mediastinal (PM) DLBCL. The BCL6 gene on chromosome 3q27 is a transcriptional repressor and is required for GC formation and function. Two molecular alterations involving the BCL6 gene are commonly observed in DLBCL: chromosomal translocations and mutations in the 5′ non-coding region. The functional consequences of BCL6 translocation and mutation have not been studied in the context of DLBCL subgroups. Therefore, we examined the frequency of translocations and the spectrum of BCL6 mutations in exon 1 and intron 1 in different DLBCL subgroups. We correlated these findings with BCL6 mRNA and protein expression, as well as the expression of BCL6 target genes. Fluorescence in situ hybridization (FISH) using a break-apart probe detected BCL6 translocations in 24 of 112 (21%) DLBCL cases. Surprisingly, the frequency of BCL6 translocation was higher in the ABC subgroup than the GCB subgroup (10 of 40; 25% vs 5 of 44; 11%, respectively) and the PM subgroup had the highest incidence (4 of 8; 50%). Expression of BCL6 protein was detected by immunohistochemistry in 75 of 138 cases (54%), including 15 of 44 (34%) in the ABC subgroup, 46 of 57 (80%) in the GCB subgroup and 4 of 10 (40%) in the PM subgroup. A good correlation of protein and mRNA expression, as assessed by cDNA microarrays (NEJM346:1937–47; 2002) was observed in the GCB subgroup but not in the other subgroups. BCL6 mutations were detected in 71 of 128 cases (55%) of DLBCL with a higher frequency in the GCB subgroup (34 of 50; 68%) and PM subgroup (10 of 12; 90%) than the ABC subgroup (14 of 43; 32%). Interestingly, there was a distinctive pattern of distribution of BCL6 mutations in the DLBCL subgroups. For example, 11 of 100 (11%) of the mutations targeted exon 1 and 8 of these 11 mutants were observed in the GCB subgroup. They preferentially affected the BCL6, STAT1 or predicted CEBP binding sites. High BCL6 mRNA and protein expression was generally associated with mutants affecting the 3′ BCL6 binding sites. We also examined the expression of 25 known BCL6 target genes in the different subgroups of DLBCL and observed the repression of this set of genes mainly in the GCB but not in the ABC subgroup, and the presence of a translocation did not correlate with target gene suppression. In conclusion, the frequency of BCL6 translocation and mutation is distinctly different in the DLBCL subgroups and BCL6 expression has different regulatory influences on target genes in different subgroups of DLBCL. Exon 1 mutations preferentially occur in the GCB subgroup and affect transcription factor binding sites. However, BCL6 translocations did not show good correlation with BCL6 expression or functional repression of target genes. The influence of the reciprocal partner genes in the translocations on the pathogenesis of DLBCL warrants further investigation.
    Print ISSN: 0006-4971
    Electronic ISSN: 1528-0020
    Topics: Biology , Medicine
    Published by American Society of Hematology
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  • 5
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    Gene Expression Distinguishes Burkitt Lymphoma from Other Aggressive Lymphomas and Identifies Patients Who Are Highly Curable with Intensive Chemotherapeutic Regimens. (2005)
    American Society of Hematology
    Details
    Publication Date: 2005-11-16
    Description: Background Burkitt lymphoma(BL) is a potentially curable, aggressive lymphoma. The distinction between BL and diffuse large B-cell lymphoma (DLBCL) is important because they differ significantly in clinical management. The distinction can be difficult because DLBCL can resemble BL in morphology, immunophenotype and cytogenetics. We investigated whether gene expression profiling (GEP) could create a molecular definition of BL that can reliably distinguish it from DLBCL. Methods Biopsy samples were collected from 312 patients with a diagnosis of sporadic BL or Burkitt-like lymphoma, or DLBCL. All cases were reviewed by a panel of expert hematopathologists. GEP of all the samples was carried out using a specialized oligonucleotide microarray. We constructed a predictor using 197 genes to distinguish BL from each molecular subtype of DLBCL. Leave-one-out cross-validation was used to evaluate the predictor’s performance. Chemotherapy treatments were grouped into either CHOP-like(CHOP, CNOP) or intensive(BFM, CODOX-M IVAC, regimens requiring stem cell rescue). Results After pathology review, the samples were reclassified as:classic BL(25 cases), atypical BL(19), DLBCL(261), and unclassifiable lymphoma(7). All classic BL and 18/19 cases of atypical BL shared a profile that was strikingly different from that of all the molecular subtypes of DLBCL, including those DLBCL cases that have a c-myc translocation. C-myc and its target genes, and genes related to germinal center differentiation were expressed at high levels in BL. NF-kB and its target genes and MHC class-I genes were expressed at very low levels in BL. Interestingly, 10 cases that were DLBCL by pathology were classified as BL by the predictor. The diagnosis of BL was supported by FISH analysis indicating a c-myc translocation. Among adults identified as having BL by the predictor (with full clinical data in N=15), overall survival was markedly superior for those receiving intensive regimens compared to CHOP-like regimens(Fig 1). The groups were similar with regard to age, stage, performance status and sites of involvement. Conclusion This study demonstrates that the molecular characteristics of BL can be used to accurately distinguish it from DLBCL. Importantly, a subgroup of BL was identified by the predictor that could not be diagnosed as BL by conventional criteria. The ability of the predictor to identify patients who benefit from aggressive therapies suggests that it will be useful in the diagnosis and management of patients with Burkitt lymphoma. Figure Figure
    Print ISSN: 0006-4971
    Electronic ISSN: 1528-0020
    Topics: Biology , Medicine
    Published by American Society of Hematology
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