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  • Mutation  (16)
  • American Association for the Advancement of Science (AAAS)  (16)
  • American Meteorological Society
  • 2015-2019  (16)
  • 2010-2014
  • 1955-1959
  • 2015  (16)
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  • 2015-2019  (16)
  • 2010-2014
  • 1955-1959
Year
  • 1
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    IMMUNODEFICIENCIES. Impairment of immunity to Candida and Mycobacterium in humans with bi-allelic RORC mutations (2015)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2015-07-15
    Description: Human inborn errors of immunity mediated by the cytokines interleukin-17A and interleukin-17F (IL-17A/F) underlie mucocutaneous candidiasis, whereas inborn errors of interferon-gamma (IFN-gamma) immunity underlie mycobacterial disease. We report the discovery of bi-allelic RORC loss-of-function mutations in seven individuals from three kindreds of different ethnic origins with both candidiasis and mycobacteriosis. The lack of functional RORgamma and RORgammaT isoforms resulted in the absence of IL-17A/F-producing T cells in these individuals, probably accounting for their chronic candidiasis. Unexpectedly, leukocytes from RORgamma- and RORgammaT-deficient individuals also displayed an impaired IFN-gamma response to Mycobacterium. This principally reflected profoundly defective IFN-gamma production by circulating gammadelta T cells and CD4(+)CCR6(+)CXCR3(+) alphabeta T cells. In humans, both mucocutaneous immunity to Candida and systemic immunity to Mycobacterium require RORgamma, RORgammaT, or both.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4668938/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4668938/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Okada, Satoshi -- Markle, Janet G -- Deenick, Elissa K -- Mele, Federico -- Averbuch, Dina -- Lagos, Macarena -- Alzahrani, Mohammed -- Al-Muhsen, Saleh -- Halwani, Rabih -- Ma, Cindy S -- Wong, Natalie -- Soudais, Claire -- Henderson, Lauren A -- Marzouqa, Hiyam -- Shamma, Jamal -- Gonzalez, Marcela -- Martinez-Barricarte, Ruben -- Okada, Chizuru -- Avery, Danielle T -- Latorre, Daniela -- Deswarte, Caroline -- Jabot-Hanin, Fabienne -- Torrado, Egidio -- Fountain, Jeffrey -- Belkadi, Aziz -- Itan, Yuval -- Boisson, Bertrand -- Migaud, Melanie -- Arlehamn, Cecilia S Lindestam -- Sette, Alessandro -- Breton, Sylvain -- McCluskey, James -- Rossjohn, Jamie -- de Villartay, Jean-Pierre -- Moshous, Despina -- Hambleton, Sophie -- Latour, Sylvain -- Arkwright, Peter D -- Picard, Capucine -- Lantz, Olivier -- Engelhard, Dan -- Kobayashi, Masao -- Abel, Laurent -- Cooper, Andrea M -- Notarangelo, Luigi D -- Boisson-Dupuis, Stephanie -- Puel, Anne -- Sallusto, Federica -- Bustamante, Jacinta -- Tangye, Stuart G -- Casanova, Jean-Laurent -- 8UL1TR000043/TR/NCATS NIH HHS/ -- HHSN272200900044C/AI/NIAID NIH HHS/ -- HHSN272200900044C/PHS HHS/ -- R37 AI095983/AI/NIAID NIH HHS/ -- R37AI095983/AI/NIAID NIH HHS/ -- T32 AI007512/AI/NIAID NIH HHS/ -- Canadian Institutes of Health Research/Canada -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2015 Aug 7;349(6248):606-13. doi: 10.1126/science.aaa4282. Epub 2015 Jul 9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉St. Giles Laboratory of Human Genetics of Infectious Diseases, Rockefeller Branch, The Rockefeller University, New York, NY 10065, USA. Department of Pediatrics, Hiroshima University Graduate School of Biomedical and Health Sciences, Hiroshima, Japan. ; St. Giles Laboratory of Human Genetics of Infectious Diseases, Rockefeller Branch, The Rockefeller University, New York, NY 10065, USA. jmarkle@rockefeller.edu jean-laurent.casanova@rockefeller.edu. ; Immunology Division, Garvan Institute of Medical Research, Darlinghurst, New South Wales, Australia. St Vincent's Clinical School, University of New South Wales, Sydney, New South Wales, Australia. ; Institute for Research in Biomedicine, University of Italian Switzerland, Bellinzona, Switzerland. ; Department of Pediatrics, Hadassah University Hospital, Jerusalem, Israel. ; Department of Immunology, School of Medicine, Universidad de Valparaiso, Santiago, Chile. Department of Pediatrics, Padre Hurtado Hospital and Clinica Alemana, Santiago, Chile. ; Department of Pediatrics, King Faisal Specialist Hospital and Research Center, Riyadh, Saudi Arabia. ; Department of Pediatrics, King Faisal Specialist Hospital and Research Center, Riyadh, Saudi Arabia. Department of Pediatrics, Prince Naif Center for Immunology Research, College of Medicine, King Saud University, Riyadh, Saudi Arabia. ; Department of Pediatrics, Prince Naif Center for Immunology Research, College of Medicine, King Saud University, Riyadh, Saudi Arabia. ; Immunology Division, Garvan Institute of Medical Research, Darlinghurst, New South Wales, Australia. ; Institut Curie, INSERM U932, Paris, France. ; Division of Immunology, Boston Children's Hospital, Boston, MA 02115, USA. ; Caritas Baby Hospital, Post Office Box 11535, Jerusalem, Israel. ; Department of Immunology, School of Medicine, Universidad de Valparaiso, Santiago, Chile. ; St. Giles Laboratory of Human Genetics of Infectious Diseases, Rockefeller Branch, The Rockefeller University, New York, NY 10065, USA. ; Laboratory of Human Genetics of Infectious Diseases, Necker Branch, INSERM UMR 1163, Paris, France. Paris Descartes University, Imagine Institute, Paris, France. ; Trudeau Institute, Saranac Lake, NY 12983, USA. ; La Jolla Institute for Allergy and Immunology, La Jolla, CA 92037, USA. ; Department of Radiology, Assistance Publique-Hopitaux de Paris (AP-HP), Necker Hospital for Sick Children, Paris, France. ; Department of Microbiology and Immunology, Peter Doherty Institute for Infection and Immunity, University of Melbourne, Parkville, Victoria, Australia. ; Department of Biochemistry and Molecular Biology, School of Biomedical Sciences, Monash University, Clayton, Victoria, Australia. Australian Research Council Centre of Excellence for Advanced Molecular Imaging, Monash University, Clayton, Victoria, Australia. Institute of Infection and Immunity, Cardiff University, School of Medicine, Heath Park, Cardiff CF14 4XN, UK. ; Laboratoire Dynamique du Genome et Systeme Immunitaire, INSERM UMR 1163, Universite Paris Descartes-Sorbonne Paris Cite, Imagine Institute, Paris, France. ; Laboratoire Dynamique du Genome et Systeme Immunitaire, INSERM UMR 1163, Universite Paris Descartes-Sorbonne Paris Cite, Imagine Institute, Paris, France. Pediatric Hematology-Immunology Unit, AP-HP, Necker Hospital for Sick Children, Paris, France. ; Institute of Cellular Medicine, Newcastle University and Great North Children's Hospital, Newcastle upon Tyne NE4 6BE, UK. ; Laboratory of Lymphocyte Activation and Susceptibility to EBV Infection, INSERM UMR 1163, Universite Paris Descartes-Sorbonne Paris Cite, Imagine Institute, Paris, France. ; Department of Paediatric Allergy Immunology, University of Manchester, Royal Manchester Children's Hospital, Manchester, UK. ; St. Giles Laboratory of Human Genetics of Infectious Diseases, Rockefeller Branch, The Rockefeller University, New York, NY 10065, USA. Laboratory of Human Genetics of Infectious Diseases, Necker Branch, INSERM UMR 1163, Paris, France. Paris Descartes University, Imagine Institute, Paris, France. Pediatric Hematology-Immunology Unit, AP-HP, Necker Hospital for Sick Children, Paris, France. Center for the Study of Primary Immunodeficiencies, AP-HP, Necker Hospital for Sick Children, Paris, France. ; Department of Pediatrics, Hiroshima University Graduate School of Biomedical and Health Sciences, Hiroshima, Japan. ; St. Giles Laboratory of Human Genetics of Infectious Diseases, Rockefeller Branch, The Rockefeller University, New York, NY 10065, USA. Laboratory of Human Genetics of Infectious Diseases, Necker Branch, INSERM UMR 1163, Paris, France. Paris Descartes University, Imagine Institute, Paris, France. ; Division of Immunology, Boston Children's Hospital, Boston, MA 02115, USA. Manton Center for Orphan Disease Research, Children's Hospital, Boston, MA 02115, USA. ; Institute for Research in Biomedicine, University of Italian Switzerland, Bellinzona, Switzerland. Center of Medical Immunology, Institute for Research in Biomedicine, University of Italian Switzerland, Bellinzona, Switzerland. ; St. Giles Laboratory of Human Genetics of Infectious Diseases, Rockefeller Branch, The Rockefeller University, New York, NY 10065, USA. Laboratory of Human Genetics of Infectious Diseases, Necker Branch, INSERM UMR 1163, Paris, France. Paris Descartes University, Imagine Institute, Paris, France. Center for the Study of Primary Immunodeficiencies, AP-HP, Necker Hospital for Sick Children, Paris, France. ; St. Giles Laboratory of Human Genetics of Infectious Diseases, Rockefeller Branch, The Rockefeller University, New York, NY 10065, USA. Laboratory of Human Genetics of Infectious Diseases, Necker Branch, INSERM UMR 1163, Paris, France. Paris Descartes University, Imagine Institute, Paris, France. Pediatric Hematology-Immunology Unit, AP-HP, Necker Hospital for Sick Children, Paris, France. Howard Hughes Medical Institute, New York, NY 10065, USA. jmarkle@rockefeller.edu jean-laurent.casanova@rockefeller.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26160376" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Animals ; Candida albicans/*immunology ; Candidiasis, Chronic Mucocutaneous/complications/*genetics/immunology ; Cattle ; Child ; Child, Preschool ; DNA Mutational Analysis ; Exome/genetics ; Female ; Gene Rearrangement, alpha-Chain T-Cell Antigen Receptor ; Humans ; Immunity/*genetics ; Interferon-gamma/immunology ; Interleukin-17/immunology ; Mice ; Mutation ; Mycobacterium bovis/immunology/isolation & purification ; Mycobacterium tuberculosis/immunology/isolation & purification ; Nuclear Receptor Subfamily 1, Group F, Member 3/*genetics ; Pedigree ; Receptors, Antigen, T-Cell, alpha-beta/genetics/immunology ; Receptors, Antigen, T-Cell, gamma-delta/genetics/immunology ; Severe Combined Immunodeficiency/*genetics ; T-Lymphocytes/immunology ; Thymus Gland/abnormalities/immunology ; Tuberculosis, Bovine/*genetics/immunology ; Tuberculosis, Pulmonary/*genetics/immunology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 2
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    Identification of an oncogenic RAB protein (2015)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2015-09-05
    Description: In a short hairpin RNA screen for genes that affect AKT phosphorylation, we identified the RAB35 small guanosine triphosphatase (GTPase)-a protein previously implicated in endomembrane trafficking-as a regulator of the phosphatidylinositol 3'-OH kinase (PI3K) pathway. Depletion of RAB35 suppresses AKT phosphorylation in response to growth factors, whereas expression of a dominant active GTPase-deficient mutant of RAB35 constitutively activates the PI3K/AKT pathway. RAB35 functions downstream of growth factor receptors and upstream of PDK1 and mTORC2 and copurifies with PI3K in immunoprecipitation assays. Two somatic RAB35 mutations found in human tumors generate alleles that constitutively activate PI3K/AKT signaling, suppress apoptosis, and transform cells in a PI3K-dependent manner. Furthermore, oncogenic RAB35 is sufficient to drive platelet-derived growth factor receptor alpha to LAMP2-positive endomembranes in the absence of ligand, suggesting that there may be latent oncogenic potential in dysregulated endomembrane trafficking.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4600465/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4600465/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wheeler, Douglas B -- Zoncu, Roberto -- Root, David E -- Sabatini, David M -- Sawyers, Charles L -- 1DP2CA195761-01/CA/NCI NIH HHS/ -- AI47389/AI/NIAID NIH HHS/ -- CA092629/CA/NCI NIH HHS/ -- CA103866/CA/NCI NIH HHS/ -- CA155169/CA/NCI NIH HHS/ -- GM07739/GM/NIGMS NIH HHS/ -- R01 CA103866/CA/NCI NIH HHS/ -- R01 CA129105/CA/NCI NIH HHS/ -- R01 CA155169/CA/NCI NIH HHS/ -- R01 CA193837/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2015 Oct 9;350(6257):211-7. doi: 10.1126/science.aaa4903. Epub 2015 Sep 3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Human Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center (MSKCC), New York, NY 10065, USA. Weill Cornell/Rockefeller University/Sloan Kettering Tri-Institutional MD-PhD Program, New York, NY 10021, USA. Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA. ; Department of Molecular and Cell Biology, University of California at Berkeley, Berkeley, CA 94720, USA. ; Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA. ; Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA. Whitehead Institute for Biomedical Research, Cambridge, MA 02142, USA. Department of Biology, Massachusetts Institute of Technology (MIT), Cambridge, MA 02142, USA. David H. Koch Institute for Integrative Cancer Research at MIT, Cambridge, MA 02142, USA. Howard Hughes Medical Institute, Chevy Chase, MD 20815, USA. sawyersc@mskcc.org sabatini@wi.mit.edu. ; Human Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center (MSKCC), New York, NY 10065, USA. Howard Hughes Medical Institute, Chevy Chase, MD 20815, USA. sawyersc@mskcc.org sabatini@wi.mit.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26338797" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Cell Line, Tumor ; Gene Deletion ; Humans ; Immunoprecipitation ; Lysosomal-Associated Membrane Protein 2/metabolism ; Multiprotein Complexes/metabolism ; Mutation ; Neoplasms/genetics/*metabolism/pathology ; Oncogene Proteins/genetics/*metabolism ; Phosphatidylinositol 3-Kinases/*metabolism ; Phosphorylation/genetics ; Protein Transport ; Protein-Serine-Threonine Kinases/metabolism ; Proto-Oncogene Proteins c-akt/metabolism ; RNA Interference ; RNA, Small Interfering/genetics ; Receptor, Platelet-Derived Growth Factor alpha/metabolism ; TOR Serine-Threonine Kinases/metabolism ; rab GTP-Binding Proteins/genetics/*metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
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    Kinase dynamics. Using ancient protein kinases to unravel a modern cancer drug's mechanism (2015)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2015-02-24
    Description: Macromolecular function is rooted in energy landscapes, where sequence determines not a single structure but an ensemble of conformations. Hence, evolution modifies a protein's function by altering its energy landscape. Here, we recreate the evolutionary pathway between two modern human oncogenes, Src and Abl, by reconstructing their common ancestors. Our evolutionary reconstruction combined with x-ray structures of the common ancestor and pre-steady-state kinetics reveals a detailed atomistic mechanism for selectivity of the successful cancer drug Gleevec. Gleevec affinity is gained during the evolutionary trajectory toward Abl and lost toward Src, primarily by shifting an induced-fit equilibrium that is also disrupted in the clinical T315I resistance mutation. This work reveals the mechanism of Gleevec specificity while offering insights into how energy landscapes evolve.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4405104/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4405104/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wilson, C -- Agafonov, R V -- Hoemberger, M -- Kutter, S -- Zorba, A -- Halpin, J -- Buosi, V -- Otten, R -- Waterman, D -- Theobald, D L -- Kern, D -- GM094468/GM/NIGMS NIH HHS/ -- GM096053/GM/NIGMS NIH HHS/ -- GM100966-01/GM/NIGMS NIH HHS/ -- R01 GM094468/GM/NIGMS NIH HHS/ -- R01 GM096053/GM/NIGMS NIH HHS/ -- R01 GM100966/GM/NIGMS NIH HHS/ -- T32 EB009419/EB/NIBIB NIH HHS/ -- T32 GM007596/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2015 Feb 20;347(6224):882-6. doi: 10.1126/science.aaa1823.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and Department of Biochemistry, Brandeis University, Waltham, MA 02452, USA. ; Department of Biochemistry, Brandeis University, Waltham, MA 02452, USA. ; Howard Hughes Medical Institute and Department of Biochemistry, Brandeis University, Waltham, MA 02452, USA. dkern@brandeis.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25700521" target="_blank"〉PubMed〈/a〉
    Keywords: Antineoplastic Agents/chemistry/*pharmacology ; Benzamides/chemistry/*pharmacology ; Drug Resistance, Neoplasm/*genetics ; Entropy ; *Evolution, Molecular ; Humans ; Imatinib Mesylate ; Mutation ; Oncogene Proteins v-abl/chemistry/genetics ; Phylogeny ; Piperazines/chemistry/*pharmacology ; Protein Binding ; Protein Kinase Inhibitors/chemistry/*pharmacology ; Protein Structure, Secondary ; Pyrimidines/chemistry/*pharmacology ; src-Family Kinases/*chemistry/classification/genetics
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 4
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    Cancer immunology. Mutational landscape determines sensitivity to PD-1 blockade in non-small cell lung cancer (2015)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2015-03-15
    Description: Immune checkpoint inhibitors, which unleash a patient's own T cells to kill tumors, are revolutionizing cancer treatment. To unravel the genomic determinants of response to this therapy, we used whole-exome sequencing of non-small cell lung cancers treated with pembrolizumab, an antibody targeting programmed cell death-1 (PD-1). In two independent cohorts, higher nonsynonymous mutation burden in tumors was associated with improved objective response, durable clinical benefit, and progression-free survival. Efficacy also correlated with the molecular smoking signature, higher neoantigen burden, and DNA repair pathway mutations; each factor was also associated with mutation burden. In one responder, neoantigen-specific CD8+ T cell responses paralleled tumor regression, suggesting that anti-PD-1 therapy enhances neoantigen-specific T cell reactivity. Our results suggest that the genomic landscape of lung cancers shapes response to anti-PD-1 therapy.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rizvi, Naiyer A -- Hellmann, Matthew D -- Snyder, Alexandra -- Kvistborg, Pia -- Makarov, Vladimir -- Havel, Jonathan J -- Lee, William -- Yuan, Jianda -- Wong, Phillip -- Ho, Teresa S -- Miller, Martin L -- Rekhtman, Natasha -- Moreira, Andre L -- Ibrahim, Fawzia -- Bruggeman, Cameron -- Gasmi, Billel -- Zappasodi, Roberta -- Maeda, Yuka -- Sander, Chris -- Garon, Edward B -- Merghoub, Taha -- Wolchok, Jedd D -- Schumacher, Ton N -- Chan, Timothy A -- K23 CA149079/CA/NCI NIH HHS/ -- P30 CA008748/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2015 Apr 3;348(6230):124-8. doi: 10.1126/science.aaa1348. Epub 2015 Mar 12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA. Weill Cornell Medical College, New York, NY, 10065, USA. chant@mskcc.org. ; Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA. Weill Cornell Medical College, New York, NY, 10065, USA. ; Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA. Weill Cornell Medical College, New York, NY, 10065, USA. Human Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA. ; Division of Immunology, Netherlands Cancer Institute, 1066 CX Amsterdam, Netherlands. ; Human Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA. ; Department of Radiation Oncology, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA. ; Immune Monitoring Core, Ludwig Center for Cancer Immunotherapy, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA. ; Computation Biology Program, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA. ; Department of Pathology, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA. ; Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA. ; Department of Mathematics, Columbia University, New York, NY, 10027, USA. ; Ludwig Collaborative Laboratory, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA. ; David Geffen School of Medicine at UCLA, 2825 Santa Monica Boulevard, Suite 200, Santa Monica, CA 90404, USA. ; Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA. Ludwig Collaborative Laboratory, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA. ; Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA. Weill Cornell Medical College, New York, NY, 10065, USA. Ludwig Collaborative Laboratory, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA. ; Weill Cornell Medical College, New York, NY, 10065, USA. Human Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA. Department of Radiation Oncology, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA. chant@mskcc.org.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25765070" target="_blank"〉PubMed〈/a〉
    Keywords: Antibodies, Monoclonal, Humanized/*therapeutic use ; Antineoplastic Agents/*therapeutic use ; CD8-Positive T-Lymphocytes/immunology ; Carcinoma, Non-Small-Cell Lung/*drug therapy/*genetics/immunology ; Cohort Studies ; DNA Repair/genetics ; Disease-Free Survival ; Drug Resistance, Neoplasm/*genetics ; Humans ; Lung Neoplasms/*drug therapy/*genetics/immunology ; Mutation ; Programmed Cell Death 1 Receptor/*antagonists & inhibitors ; Smoking/genetics
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 5
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    Genomic correlates of response to CTLA-4 blockade in metastatic melanoma (2015)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2015-09-12
    Description: Monoclonal antibodies directed against cytotoxic T lymphocyte-associated antigen-4 (CTLA-4), such as ipilimumab, yield considerable clinical benefit for patients with metastatic melanoma by inhibiting immune checkpoint activity, but clinical predictors of response to these therapies remain incompletely characterized. To investigate the roles of tumor-specific neoantigens and alterations in the tumor microenvironment in the response to ipilimumab, we analyzed whole exomes from pretreatment melanoma tumor biopsies and matching germline tissue samples from 110 patients. For 40 of these patients, we also obtained and analyzed transcriptome data from the pretreatment tumor samples. Overall mutational load, neoantigen load, and expression of cytolytic markers in the immune microenvironment were significantly associated with clinical benefit. However, no recurrent neoantigen peptide sequences predicted responder patient populations. Thus, detailed integrated molecular characterization of large patient cohorts may be needed to identify robust determinants of response and resistance to immune checkpoint inhibitors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Van Allen, Eliezer M -- Miao, Diana -- Schilling, Bastian -- Shukla, Sachet A -- Blank, Christian -- Zimmer, Lisa -- Sucker, Antje -- Hillen, Uwe -- Foppen, Marnix H Geukes -- Goldinger, Simone M -- Utikal, Jochen -- Hassel, Jessica C -- Weide, Benjamin -- Kaehler, Katharina C -- Loquai, Carmen -- Mohr, Peter -- Gutzmer, Ralf -- Dummer, Reinhard -- Gabriel, Stacey -- Wu, Catherine J -- Schadendorf, Dirk -- Garraway, Levi A -- U54 HG003067/HG/NHGRI NIH HHS/ -- New York, N.Y. -- Science. 2015 Oct 9;350(6257):207-11. doi: 10.1126/science.aad0095. Epub 2015 Sep 10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA 02215, USA. Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA. Center for Cancer Precision Medicine, Dana-Farber Cancer Institute, Boston, MA 02215, USA. ; Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA 02215, USA. Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA. ; Department of Dermatology, University Hospital, University Duisburg-Essen, 45147 Essen, Germany. German Cancer Consortium(DKTK), 69121 Heidelberg, Germany. ; Department of Medical Oncology, Netherlands Cancer Institute, 1066 CX Amsterdam, Netherlands. ; Department of Dermatology, University Hospital Zurich, 8091 Zurich, Switzerland. ; Skin Cancer Unit, German Cancer Research Center(DKTK), 69121 Heidelberg, Germany. Skin Cancer Unit, German Cancer Research Center(DKTK), 69121 Heidelberg, Germany. Department of Dermatology, Venerology, and Allergology, University Medical Center, Ruprecht-Karls University of Heidelberg, 68167 Mannheim, Germany. ; Department of Dermatology, University Hospital, Ruprecht-Karls University of Heidelberg, 69120 Heidelberg, Germany. ; Department of Dermatology, University Hospital Tubingen, 72076 Tubingen, Germany. ; Department of Dermatology, University Hospital Kiel, 24105 Kiel, Germany. ; Department of Dermatology, University Medical Center, 55131 Mainz, Germany. ; Department of Dermatology, Elbe-Kliniken, 21614 Buxtehude, Germany. ; Department of Dermatology and Allergy, Skin Cancer Center Hannover, Hannover Medical School, 30625 Hannover, Germany. ; Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA. ; Department of Dermatology, University Hospital, University Duisburg-Essen, 45147 Essen, Germany. German Cancer Consortium(DKTK), 69121 Heidelberg, Germany. levi_garraway@dfci.harvard.edu dirk.schadendorf@uk-essen.de. ; Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA 02215, USA. Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA. Center for Cancer Precision Medicine, Dana-Farber Cancer Institute, Boston, MA 02215, USA. levi_garraway@dfci.harvard.edu dirk.schadendorf@uk-essen.de.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26359337" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Aged ; Aged, 80 and over ; Antibodies, Monoclonal/*pharmacology/therapeutic use ; Antigens, Neoplasm/*genetics ; *Biomarkers, Pharmacological ; CTLA-4 Antigen/*antagonists & inhibitors ; Cell Cycle Checkpoints/genetics/immunology ; Cohort Studies ; DNA Mutational Analysis ; Drug Resistance, Neoplasm/genetics ; Exome ; Female ; Genomics ; HLA Antigens/genetics ; Humans ; Male ; Melanoma/*drug therapy/*genetics/secondary ; Middle Aged ; Mutation ; Skin Neoplasms/*drug therapy/*genetics/pathology ; Tumor Microenvironment/drug effects/immunology ; Young Adult
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 6
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    RNA biochemistry. Determination of in vivo target search kinetics of regulatory noncoding RNA (2015)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2015-03-21
    Description: Base-pairing interactions between nucleic acids mediate target recognition in many biological processes. We developed a super-resolution imaging and modeling platform that enabled the in vivo determination of base pairing-mediated target recognition kinetics. We examined a stress-induced bacterial small RNA, SgrS, which induces the degradation of target messenger RNAs (mRNAs). SgrS binds to a primary target mRNA in a reversible and dynamic fashion, and formation of SgrS-mRNA complexes is rate-limiting, dictating the overall regulation efficiency in vivo. Examination of a secondary target indicated that differences in the target search kinetics contribute to setting the regulation priority among different target mRNAs. This super-resolution imaging and analysis approach provides a conceptual framework that can be generalized to other small RNA systems and other target search processes.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4410144/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4410144/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fei, Jingyi -- Singh, Digvijay -- Zhang, Qiucen -- Park, Seongjin -- Balasubramanian, Divya -- Golding, Ido -- Vanderpool, Carin K -- Ha, Taekjip -- GM 112659/GM/NIGMS NIH HHS/ -- GM065367/GM/NIGMS NIH HHS/ -- GM082837/GM/NIGMS NIH HHS/ -- GM092830/GM/NIGMS NIH HHS/ -- R01 GM065367/GM/NIGMS NIH HHS/ -- R01 GM082837/GM/NIGMS NIH HHS/ -- R01 GM092830/GM/NIGMS NIH HHS/ -- R01 GM112659/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2015 Mar 20;347(6228):1371-4. doi: 10.1126/science.1258849.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for the Physics of Living Cells, Department of Physics, University of Illinois, Urbana, IL, USA. ; Center for Biophysics and Computational Biology, University of Illinois, Urbana, IL, USA. ; Department of Microbiology, University of Illinois, Urbana, IL, USA. ; Center for the Physics of Living Cells, Department of Physics, University of Illinois, Urbana, IL, USA. Verna and Marrs McLean Department of Biochemistry and Molecular Biology, Baylor College of Medicine, Houston, TX, USA. ; Department of Microbiology, University of Illinois, Urbana, IL, USA. tjha@illinois.edu cvanderp@life.uiuc.edu. ; Center for the Physics of Living Cells, Department of Physics, University of Illinois, Urbana, IL, USA. Center for Biophysics and Computational Biology, University of Illinois, Urbana, IL, USA. Carl R. Woese Institute for Genomic Biology, Howard Hughes Medical Institute, Urbana, IL, USA. Howard Hughes Medical Institute, Urbana, IL, USA. tjha@illinois.edu cvanderp@life.uiuc.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25792329" target="_blank"〉PubMed〈/a〉
    Keywords: *Base Pairing ; Endoribonucleases/chemistry/genetics ; Escherichia coli/genetics/metabolism ; Kinetics ; Molecular Imaging/*methods ; Mutation ; Phosphoenolpyruvate Sugar Phosphotransferase System/genetics ; *RNA Stability ; RNA, Messenger/*chemistry ; RNA, Small Untranslated/*chemistry
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  • 7
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    Infectious disease. Life-threatening influenza and impaired interferon amplification in human IRF7 deficiency (2015)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2015-03-31
    Description: Severe influenza disease strikes otherwise healthy children and remains unexplained. We report compound heterozygous null mutations in IRF7, which encodes the transcription factor interferon regulatory factor 7, in an otherwise healthy child who suffered life-threatening influenza during primary infection. In response to influenza virus, the patient's leukocytes and plasmacytoid dendritic cells produced very little type I and III interferons (IFNs). Moreover, the patient's dermal fibroblasts and induced pluripotent stem cell (iPSC)-derived pulmonary epithelial cells produced reduced amounts of type I IFN and displayed increased influenza virus replication. These findings suggest that IRF7-dependent amplification of type I and III IFNs is required for protection against primary infection by influenza virus in humans. They also show that severe influenza may result from single-gene inborn errors of immunity.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4431581/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4431581/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ciancanelli, Michael J -- Huang, Sarah X L -- Luthra, Priya -- Garner, Hannah -- Itan, Yuval -- Volpi, Stefano -- Lafaille, Fabien G -- Trouillet, Celine -- Schmolke, Mirco -- Albrecht, Randy A -- Israelsson, Elisabeth -- Lim, Hye Kyung -- Casadio, Melina -- Hermesh, Tamar -- Lorenzo, Lazaro -- Leung, Lawrence W -- Pedergnana, Vincent -- Boisson, Bertrand -- Okada, Satoshi -- Picard, Capucine -- Ringuier, Benedicte -- Troussier, Francoise -- Chaussabel, Damien -- Abel, Laurent -- Pellier, Isabelle -- Notarangelo, Luigi D -- Garcia-Sastre, Adolfo -- Basler, Christopher F -- Geissmann, Frederic -- Zhang, Shen-Ying -- Snoeck, Hans-Willem -- Casanova, Jean-Laurent -- 1U19AI109945/AI/NIAID NIH HHS/ -- 5R01AI100887/AI/NIAID NIH HHS/ -- 5R01NS072381/NS/NINDS NIH HHS/ -- 8UL1TR000043/TR/NCATS NIH HHS/ -- HHSN272201400008C/PHS HHS/ -- R01 AI100887/AI/NIAID NIH HHS/ -- R01 NS072381/NS/NINDS NIH HHS/ -- U19 AI109945/AI/NIAID NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2015 Apr 24;348(6233):448-53. doi: 10.1126/science.aaa1578. Epub 2015 Mar 26.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉St. Giles Laboratory of Human Genetics of Infectious Diseases, Rockefeller Branch, The Rockefeller University, New York, NY, USA. ; Columbia Center for Translational Immunology, Columbia University Medical Center, New York, NY, USA. Department of Medicine, Columbia University Medical Center, New York, NY, USA. ; Department of Microbiology, Icahn School of Medicine at Mount Sinai, New York, NY, USA. ; Centre for Molecular and Cellular Biology of Inflammation (CMCBI), King's College London, London SE1 1UL, UK. ; Division of Immunology and Manton Center for Orphan Disease Research, Children's Hospital, Harvard Medical School, Boston, MA, USA. Department of Neuroscience, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health, University of Genoa, 16132 Genoa, Italy. ; Department of Microbiology, Icahn School of Medicine at Mount Sinai, New York, NY, USA. Global Health and Emerging Pathogens Institute, Icahn School of Medicine at Mount Sinai, New York, NY, USA. ; Department of Systems Immunology, Benaroya Research Institute at Virginia Mason, Seattle, WA, USA. ; Laboratory of Human Genetics of Infectious Diseases, Necker Branch, INSERM UMR1163, Paris, France. University Paris Descartes, Imagine Institute, Paris, France. ; St. Giles Laboratory of Human Genetics of Infectious Diseases, Rockefeller Branch, The Rockefeller University, New York, NY, USA. Department of Pediatrics, Hiroshima University Graduate School of Biomedical & Health Sciences, Hiroshima, Japan. ; St. Giles Laboratory of Human Genetics of Infectious Diseases, Rockefeller Branch, The Rockefeller University, New York, NY, USA. Laboratory of Human Genetics of Infectious Diseases, Necker Branch, INSERM UMR1163, Paris, France. University Paris Descartes, Imagine Institute, Paris, France. Study Centre for Primary Immunodeficiencies, AP-HP, Necker Hospital, Paris, France. ; Pediatric Intensive Care Unit, University Hospital, Angers, France. ; General Pediatrics Unit, University Hospital, Angers, France. ; Department of Systems Immunology, Benaroya Research Institute at Virginia Mason, Seattle, WA, USA. Department of Systems Biology, Sidra Medical and Research Center, Doha, Qatar. ; St. Giles Laboratory of Human Genetics of Infectious Diseases, Rockefeller Branch, The Rockefeller University, New York, NY, USA. Laboratory of Human Genetics of Infectious Diseases, Necker Branch, INSERM UMR1163, Paris, France. University Paris Descartes, Imagine Institute, Paris, France. ; Pediatric Immunology, Hematology and Oncology Unit, University Hospital Centre of Angers, Angers, France. INSERM U892, CNRS U6299, Angers, France. ; Division of Immunology and Manton Center for Orphan Disease Research, Children's Hospital, Harvard Medical School, Boston, MA, USA. ; Department of Microbiology, Icahn School of Medicine at Mount Sinai, New York, NY, USA. Global Health and Emerging Pathogens Institute, Icahn School of Medicine at Mount Sinai, New York, NY, USA. Department of Medicine, Division of Infectious Diseases, Icahn School of Medicine at Mount Sinai, New York, NY, USA. ; St. Giles Laboratory of Human Genetics of Infectious Diseases, Rockefeller Branch, The Rockefeller University, New York, NY, USA. Laboratory of Human Genetics of Infectious Diseases, Necker Branch, INSERM UMR1163, Paris, France. University Paris Descartes, Imagine Institute, Paris, France. Pediatric Immuno-Hematology Unit, Necker Hospital for Sick Children, AP-HP, Paris, France. Howard Hughes Medical Institute, New York, NY, USA. jean-laurent.casanova@rockefeller.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25814066" target="_blank"〉PubMed〈/a〉
    Keywords: Child ; Dendritic Cells/immunology ; Female ; Fibroblasts/immunology ; Genes, Recessive ; *Heterozygote ; Humans ; Induced Pluripotent Stem Cells/immunology ; *Influenza A Virus, H1N1 Subtype ; Influenza, Human/complications/genetics/*immunology ; Interferon Regulatory Factor-7/*genetics ; Interferon Type I/*biosynthesis/genetics ; Leukocytes/immunology ; Lung/immunology ; Mutation ; Respiratory Distress Syndrome, Adult/genetics/*immunology/virology ; Respiratory Mucosa/immunology
    Print ISSN: 0036-8075
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  • 8
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    EVOLUTION. Fruit flies diversify their offspring in response to parasite infection (2015)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2015-08-15
    Description: The evolution of sexual reproduction is often explained by Red Queen dynamics: Organisms must continually evolve to maintain fitness relative to interacting organisms, such as parasites. Recombination accompanies sexual reproduction and helps diversify an organism's offspring, so that parasites cannot exploit static host genotypes. Here we show that Drosophila melanogaster plastically increases the production of recombinant offspring after infection. The response is consistent across genetic backgrounds, developmental stages, and parasite types but is not induced after sterile wounding. Furthermore, the response appears to be driven by transmission distortion rather than increased recombination. Our study extends the Red Queen model to include the increased production of recombinant offspring and uncovers a remarkable ability of hosts to actively distort their recombination fraction in rapid response to environmental cues.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Singh, Nadia D -- Criscoe, Dallas R -- Skolfield, Shelly -- Kohl, Kathryn P -- Keebaugh, Erin S -- Schlenke, Todd A -- New York, N.Y. -- Science. 2015 Aug 14;349(6249):747-50. doi: 10.1126/science.aab1768.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Sciences and Bioinformatics Research Center, North Carolina State University, Raleigh, NC, USA. ndsingh@ncsu.edu schlenkt@reed.edu. ; Translational Biology and Molecular Medicine Program, Baylor College of Medicine, Houston, TX, USA. ; Department of Biology, Reed College, Portland, OR, USA. ; Department of Biology, Winthrop University, Rock Hill, SC, USA. ; Department of Biology, Emory University, Atlanta, GA, USA. ; Department of Biology, Reed College, Portland, OR, USA. ndsingh@ncsu.edu schlenkt@reed.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26273057" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biological Evolution ; Drosophila melanogaster/*genetics/growth & development/*parasitology ; Female ; *Genetic Fitness ; Genetic Variation ; Larva ; Male ; Mutation ; Parasitic Diseases/genetics ; *Recombination, Genetic ; Reproduction/genetics
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  • 9
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    Crystal structure of the anion exchanger domain of human erythrocyte band 3 (2015)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2015-11-07
    Description: Anion exchanger 1 (AE1), also known as band 3 or SLC4A1, plays a key role in the removal of carbon dioxide from tissues by facilitating the exchange of chloride and bicarbonate across the plasma membrane of erythrocytes. An isoform of AE1 is also present in the kidney. Specific mutations in human AE1 cause several types of hereditary hemolytic anemias and/or distal renal tubular acidosis. Here we report the crystal structure of the band 3 anion exchanger domain (AE1(CTD)) at 3.5 angstroms. The structure is locked in an outward-facing open conformation by an inhibitor. Comparing this structure with a substrate-bound structure of the uracil transporter UraA in an inward-facing conformation allowed us to identify the anion-binding position in the AE1(CTD), and to propose a possible transport mechanism that could explain why selected mutations lead to disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Arakawa, Takatoshi -- Kobayashi-Yurugi, Takami -- Alguel, Yilmaz -- Iwanari, Hiroko -- Hatae, Hinako -- Iwata, Momi -- Abe, Yoshito -- Hino, Tomoya -- Ikeda-Suno, Chiyo -- Kuma, Hiroyuki -- Kang, Dongchon -- Murata, Takeshi -- Hamakubo, Takao -- Cameron, Alexander D -- Kobayashi, Takuya -- Hamasaki, Naotaka -- Iwata, So -- BB/D019516/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- BB/G023425/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- WT089809/Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2015 Nov 6;350(6261):680-4. doi: 10.1126/science.aaa4335.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Japan Science and Technology Agency (JST), Exploratory Research for Advanced Technology (ERATO) Human Receptor Crystallography Project, Konoe-cho, Yoshida, Sakyo-ku, Kyoto 606-8501, Japan. JST, Research Acceleration Program, Membrane Protein Crystallography Project, Konoe-cho, Yoshida, Sakyo-ku, Kyoto 606-8501, Japan. Department of Cell Biology, Kyoto University Faculty of Medicine, Konoe-cho, Yoshida, Sakyo-ku, Kyoto 606-8501, Japan. ; Japan Science and Technology Agency (JST), Exploratory Research for Advanced Technology (ERATO) Human Receptor Crystallography Project, Konoe-cho, Yoshida, Sakyo-ku, Kyoto 606-8501, Japan. Department of Cell Biology, Kyoto University Faculty of Medicine, Konoe-cho, Yoshida, Sakyo-ku, Kyoto 606-8501, Japan. ; Division of Molecular Biosciences, Membrane Protein Crystallography group, Imperial College London, London SW7 2AZ, UK. Membrane Protein Laboratory, Diamond Light Source, Harwell Science and Innovation Campus, Didcot, Chilton, Oxfordshire OX11 0DE, UK. Research Complex at Harwell Rutherford, Appleton Laboratory, Harwell Oxford, Didcot, Oxfordshire OX11 0FA, UK. ; Department of Quantitative Biology and Medicine, Research Center for Advanced Science and Technology, The University of Tokyo, 4-6-1 Komaba, Meguro-ku, Tokyo 153-8904, Japan. ; Faculty of Pharmaceutical Sciences, Nagasaki International University, 2825-7 Huis Ten Bosch-cho, Sasebo, Nagasaki 859-3298, Japan. ; Division of Molecular Biosciences, Membrane Protein Crystallography group, Imperial College London, London SW7 2AZ, UK. Membrane Protein Laboratory, Diamond Light Source, Harwell Science and Innovation Campus, Didcot, Chilton, Oxfordshire OX11 0DE, UK. ; Department of Protein Structure, Function and Design, Graduate School of Pharmaceutical Sciences, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka 812-8582, Japan. ; Department of Clinical Chemistry and Laboratory Medicine, Graduate School of Medical Sciences, Kyushu University, Fukuoka 812-8582, Japan. ; Japan Science and Technology Agency (JST), Exploratory Research for Advanced Technology (ERATO) Human Receptor Crystallography Project, Konoe-cho, Yoshida, Sakyo-ku, Kyoto 606-8501, Japan. Department of Cell Biology, Kyoto University Faculty of Medicine, Konoe-cho, Yoshida, Sakyo-ku, Kyoto 606-8501, Japan. Department of Chemistry, Graduate School of Science, Chiba University, 1-33 Yayoi-cho, Inage, Chiba 263-8522, Japan. ; Japan Science and Technology Agency (JST), Exploratory Research for Advanced Technology (ERATO) Human Receptor Crystallography Project, Konoe-cho, Yoshida, Sakyo-ku, Kyoto 606-8501, Japan. Division of Molecular Biosciences, Membrane Protein Crystallography group, Imperial College London, London SW7 2AZ, UK. Membrane Protein Laboratory, Diamond Light Source, Harwell Science and Innovation Campus, Didcot, Chilton, Oxfordshire OX11 0DE, UK. Research Complex at Harwell Rutherford, Appleton Laboratory, Harwell Oxford, Didcot, Oxfordshire OX11 0FA, UK. School of Life Sciences, University of Warwick, Gibbet Hill Road, Coventry CV4 7AL, UK. ; Japan Science and Technology Agency (JST), Exploratory Research for Advanced Technology (ERATO) Human Receptor Crystallography Project, Konoe-cho, Yoshida, Sakyo-ku, Kyoto 606-8501, Japan. JST, Research Acceleration Program, Membrane Protein Crystallography Project, Konoe-cho, Yoshida, Sakyo-ku, Kyoto 606-8501, Japan. Department of Cell Biology, Kyoto University Faculty of Medicine, Konoe-cho, Yoshida, Sakyo-ku, Kyoto 606-8501, Japan. Platform for Drug Discovery, Informatics, and Structural Life Science, Konoe-cho, Yoshida, Sakyo-ku, Kyoto 606-8501, Japan. ; Japan Science and Technology Agency (JST), Exploratory Research for Advanced Technology (ERATO) Human Receptor Crystallography Project, Konoe-cho, Yoshida, Sakyo-ku, Kyoto 606-8501, Japan. JST, Research Acceleration Program, Membrane Protein Crystallography Project, Konoe-cho, Yoshida, Sakyo-ku, Kyoto 606-8501, Japan. Department of Cell Biology, Kyoto University Faculty of Medicine, Konoe-cho, Yoshida, Sakyo-ku, Kyoto 606-8501, Japan. Division of Molecular Biosciences, Membrane Protein Crystallography group, Imperial College London, London SW7 2AZ, UK. Membrane Protein Laboratory, Diamond Light Source, Harwell Science and Innovation Campus, Didcot, Chilton, Oxfordshire OX11 0DE, UK. Research Complex at Harwell Rutherford, Appleton Laboratory, Harwell Oxford, Didcot, Oxfordshire OX11 0FA, UK. Platform for Drug Discovery, Informatics, and Structural Life Science, Konoe-cho, Yoshida, Sakyo-ku, Kyoto 606-8501, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26542571" target="_blank"〉PubMed〈/a〉
    Keywords: Anion Exchange Protein 1, Erythrocyte/*chemistry/genetics ; Crystallography, X-Ray ; Disease/genetics ; Escherichia coli Proteins/chemistry ; Humans ; Membrane Transport Proteins/chemistry ; Mutation ; Protein Structure, Secondary ; Protein Structure, Tertiary
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  • 10
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    Neoantigens in cancer immunotherapy (2015)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2015-04-04
    Description: The clinical relevance of T cells in the control of a diverse set of human cancers is now beyond doubt. However, the nature of the antigens that allow the immune system to distinguish cancer cells from noncancer cells has long remained obscure. Recent technological innovations have made it possible to dissect the immune response to patient-specific neoantigens that arise as a consequence of tumor-specific mutations, and emerging data suggest that recognition of such neoantigens is a major factor in the activity of clinical immunotherapies. These observations indicate that neoantigen load may form a biomarker in cancer immunotherapy and provide an incentive for the development of novel therapeutic approaches that selectively enhance T cell reactivity against this class of antigens.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schumacher, Ton N -- Schreiber, Robert D -- R01CA04305926/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2015 Apr 3;348(6230):69-74. doi: 10.1126/science.aaa4971.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Immunology, Netherlands Cancer Institute, Plesmanlaan 121, 1066 CX, Amsterdam, Netherlands. t.schumacher@nki.nl schreiber@immunology.wustl.edu. ; Department of Pathology and Immunology, Washington University School of Medicine, 660 South Euclid Avenue, St. Louis, MO 63110, USA. t.schumacher@nki.nl schreiber@immunology.wustl.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25838375" target="_blank"〉PubMed〈/a〉
    Keywords: Antigens, Neoplasm/genetics/*immunology ; Biomarkers, Tumor/genetics/*immunology ; DNA Mutational Analysis ; Exome ; Female ; Genes, Neoplasm ; Humans ; Immunotherapy/*methods ; Mutation ; Neoplasms/genetics/immunology/*therapy ; T-Lymphocytes/*immunology
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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