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  • 1
    Publication Date: 2005-07-16
    Description: African trypanosomes cause human sleeping sickness and livestock trypanosomiasis in sub-Saharan Africa. We present the sequence and analysis of the 11 megabase-sized chromosomes of Trypanosoma brucei. The 26-megabase genome contains 9068 predicted genes, including approximately 900 pseudogenes and approximately 1700 T. brucei-specific genes. Large subtelomeric arrays contain an archive of 806 variant surface glycoprotein (VSG) genes used by the parasite to evade the mammalian immune system. Most VSG genes are pseudogenes, which may be used to generate expressed mosaic genes by ectopic recombination. Comparisons of the cytoskeleton and endocytic trafficking systems with those of humans and other eukaryotic organisms reveal major differences. A comparison of metabolic pathways encoded by the genomes of T. brucei, T. cruzi, and Leishmania major reveals the least overall metabolic capability in T. brucei and the greatest in L. major. Horizontal transfer of genes of bacterial origin has contributed to some of the metabolic differences in these parasites, and a number of novel potential drug targets have been identified.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Berriman, Matthew -- Ghedin, Elodie -- Hertz-Fowler, Christiane -- Blandin, Gaelle -- Renauld, Hubert -- Bartholomeu, Daniella C -- Lennard, Nicola J -- Caler, Elisabet -- Hamlin, Nancy E -- Haas, Brian -- Bohme, Ulrike -- Hannick, Linda -- Aslett, Martin A -- Shallom, Joshua -- Marcello, Lucio -- Hou, Lihua -- Wickstead, Bill -- Alsmark, U Cecilia M -- Arrowsmith, Claire -- Atkin, Rebecca J -- Barron, Andrew J -- Bringaud, Frederic -- Brooks, Karen -- Carrington, Mark -- Cherevach, Inna -- Chillingworth, Tracey-Jane -- Churcher, Carol -- Clark, Louise N -- Corton, Craig H -- Cronin, Ann -- Davies, Rob M -- Doggett, Jonathon -- Djikeng, Appolinaire -- Feldblyum, Tamara -- Field, Mark C -- Fraser, Audrey -- Goodhead, Ian -- Hance, Zahra -- Harper, David -- Harris, Barbara R -- Hauser, Heidi -- Hostetler, Jessica -- Ivens, Al -- Jagels, Kay -- Johnson, David -- Johnson, Justin -- Jones, Kristine -- Kerhornou, Arnaud X -- Koo, Hean -- Larke, Natasha -- Landfear, Scott -- Larkin, Christopher -- Leech, Vanessa -- Line, Alexandra -- Lord, Angela -- Macleod, Annette -- Mooney, Paul J -- Moule, Sharon -- Martin, David M A -- Morgan, Gareth W -- Mungall, Karen -- Norbertczak, Halina -- Ormond, Doug -- Pai, Grace -- Peacock, Chris S -- Peterson, Jeremy -- Quail, Michael A -- Rabbinowitsch, Ester -- Rajandream, Marie-Adele -- Reitter, Chris -- Salzberg, Steven L -- Sanders, Mandy -- Schobel, Seth -- Sharp, Sarah -- Simmonds, Mark -- Simpson, Anjana J -- Tallon, Luke -- Turner, C Michael R -- Tait, Andrew -- Tivey, Adrian R -- Van Aken, Susan -- Walker, Danielle -- Wanless, David -- Wang, Shiliang -- White, Brian -- White, Owen -- Whitehead, Sally -- Woodward, John -- Wortman, Jennifer -- Adams, Mark D -- Embley, T Martin -- Gull, Keith -- Ullu, Elisabetta -- Barry, J David -- Fairlamb, Alan H -- Opperdoes, Fred -- Barrell, Barclay G -- Donelson, John E -- Hall, Neil -- Fraser, Claire M -- Melville, Sara E -- El-Sayed, Najib M -- AI43062/AI/NIAID NIH HHS/ -- R01 AI043062/AI/NIAID NIH HHS/ -- U01 AI043062/AI/NIAID NIH HHS/ -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2005 Jul 15;309(5733):416-22.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton CB10 1SA, UK. mb4@sanger.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16020726" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acids/metabolism ; Animals ; Antigenic Variation ; Antigens, Protozoan/chemistry/genetics/immunology ; Carbohydrate Metabolism ; Chromosomes/genetics ; Cytoskeleton/chemistry/genetics/physiology ; Ergosterol/biosynthesis ; Genes, Protozoan ; *Genome, Protozoan ; Glutathione/*analogs & derivatives/metabolism ; Glycosylphosphatidylinositols/biosynthesis ; Humans ; Lipid Metabolism ; Molecular Sequence Data ; Protein Transport ; Protozoan Proteins/chemistry/*genetics/metabolism ; Pseudogenes ; Purines/metabolism ; Pyrimidines/biosynthesis ; Recombination, Genetic ; *Sequence Analysis, DNA ; Spermidine/*analogs & derivatives/metabolism ; Trypanosoma brucei brucei/chemistry/*genetics/immunology/metabolism ; Trypanosomiasis, African/parasitology
    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
    Publication Date: 1999-04-24
    Description: The lack of an adequate hominid fossil record in eastern Africa between 2 and 3 million years ago (Ma) has hampered investigations of early hominid phylogeny. Discovery of 2.5 Ma hominid cranial and dental remains from the Hata beds of Ethiopia's Middle Awash allows recognition of a new species of Australopithecus. This species is descended from Australopithecus afarensis and is a candidate ancestor for early Homo. Contemporary postcranial remains feature a derived humanlike humeral/femoral ratio and an apelike upper arm-to-lower arm ratio.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Asfaw, B -- White, T -- Lovejoy, O -- Latimer, B -- Simpson, S -- Suwa, G -- New York, N.Y. -- Science. 1999 Apr 23;284(5414):629-35.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Rift Valley Research Service, Post Office Box 5717, Addis Ababa, Ethiopia.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10213683" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biological Evolution ; Bones of Upper Extremity/anatomy & histology ; Dentition ; Ethiopia ; *Fossils ; History, Ancient ; Hominidae/anatomy & histology/*classification ; Humans ; Leg Bones/anatomy & histology ; Paleodontology ; Phylogeny ; Skull/anatomy & histology ; Terminology as Topic ; Tooth/anatomy & histology
    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
    Publication Date: 1999-04-24
    Description: The Hata Member of the Bouri Formation is defined for Pliocene sedimentary outcrops in the Middle Awash Valley, Ethiopia. The Hata Member is dated to 2.5 million years ago and has produced a new species of Australopithecus and hominid postcranial remains not currently assigned to species. Spatially associated zooarchaeological remains show that hominids acquired meat and marrow by 2.5 million years ago and that they are the near contemporary of Oldowan artifacts at nearby Gona. The combined evidence suggests that behavioral changes associated with lithic technology and enhanced carnivory may have been coincident with the emergence of the Homo clade from Australopithecus afarensis in eastern Africa.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉de Heinzelin, J -- Clark, J D -- White, T -- Hart, W -- Renne, P -- WoldeGabriel, G -- Beyene, Y -- Vrba, E -- New York, N.Y. -- Science. 1999 Apr 23;284(5414):625-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institut Royal des Sciences Naturelles de Belgique, Rue Vautier 29, B-1000 Bruxelles, Belgium.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10213682" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Diet ; Ethiopia ; *Fossils ; *Geologic Sediments ; History, Ancient ; *Hominidae ; Humans
    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
    Publication Date: 1999-10-03
    Description: The cave site of Moula-Guercy, 80 meters above the modern Rhone River, was occupied by Neanderthals approximately 100,000 years ago. Excavations since 1991 have yielded rich paleontological, paleobotanical, and archaeological assemblages, including parts of six Neanderthals. The Neanderthals are contemporary with stone tools and faunal remains in the same tightly controlled stratigraphic and spatial contexts. The inference of Neanderthal cannibalism at Moula-Guercy is based on comparative analysis of hominid and ungulate bone spatial distributions, modifications by stone tools, and skeletal part representations.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Defleur, A -- White, T -- Valensi, P -- Slimak, L -- Cregut-Bonnoure, E -- New York, N.Y. -- Science. 1999 Oct 1;286(5437):128-31.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉UMR 6569 du CNRS, Laboratoire d'Anthropologie, Faculte de Medecine, Secteur Nord, Boulevard Pierre Dramart, 13916 Marseille Cedex 20, France. defleur@voltaire.timone.univ-mrs.fr〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10506562" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Archaeology ; Bone and Bones/anatomy & histology ; Cannibalism/*history ; Deer ; *Fossils ; France ; History, Ancient ; *Hominidae ; Humans
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  • 5
    Publication Date: 2000-03-10
    Description: The 2,272,351-base pair genome of Neisseria meningitidis strain MC58 (serogroup B), a causative agent of meningitis and septicemia, contains 2158 predicted coding regions, 1158 (53.7%) of which were assigned a biological role. Three major islands of horizontal DNA transfer were identified; two of these contain genes encoding proteins involved in pathogenicity, and the third island contains coding sequences only for hypothetical proteins. Insights into the commensal and virulence behavior of N. meningitidis can be gleaned from the genome, in which sequences for structural proteins of the pilus are clustered and several coding regions unique to serogroup B capsular polysaccharide synthesis can be identified. Finally, N. meningitidis contains more genes that undergo phase variation than any pathogen studied to date, a mechanism that controls their expression and contributes to the evasion of the host immune system.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tettelin, H -- Saunders, N J -- Heidelberg, J -- Jeffries, A C -- Nelson, K E -- Eisen, J A -- Ketchum, K A -- Hood, D W -- Peden, J F -- Dodson, R J -- Nelson, W C -- Gwinn, M L -- DeBoy, R -- Peterson, J D -- Hickey, E K -- Haft, D H -- Salzberg, S L -- White, O -- Fleischmann, R D -- Dougherty, B A -- Mason, T -- Ciecko, A -- Parksey, D S -- Blair, E -- Cittone, H -- Clark, E B -- Cotton, M D -- Utterback, T R -- Khouri, H -- Qin, H -- Vamathevan, J -- Gill, J -- Scarlato, V -- Masignani, V -- Pizza, M -- Grandi, G -- Sun, L -- Smith, H O -- Fraser, C M -- Moxon, E R -- Rappuoli, R -- Venter, J C -- New York, N.Y. -- Science. 2000 Mar 10;287(5459):1809-15.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Institute for Genomic Research (TIGR), 9712 Medical Center Drive, Rockville, MD 20850, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10710307" target="_blank"〉PubMed〈/a〉
    Keywords: Antigenic Variation ; Antigens, Bacterial/immunology ; Bacteremia/microbiology ; Bacterial Capsules/genetics ; Bacterial Proteins/genetics/physiology ; DNA Transposable Elements ; Evolution, Molecular ; Fimbriae, Bacterial/genetics ; *Genome, Bacterial ; Humans ; Meningitis, Meningococcal/microbiology ; Meningococcal Infections/microbiology ; Molecular Sequence Data ; Mutation ; Neisseria meningitidis/classification/*genetics/*pathogenicity/physiology ; Open Reading Frames ; Operon ; Phylogeny ; Recombination, Genetic ; *Sequence Analysis, DNA ; Serotyping ; Transformation, Bacterial ; Virulence/genetics
    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
    Publication Date: 1999-03-26
    Description: Dysregulation of Wnt-beta-catenin signaling disrupts axis formation in vertebrate embryos and underlies multiple human malignancies. The adenomatous polyposis coli (APC) protein, axin, and glycogen synthase kinase 3beta form a Wnt-regulated signaling complex that mediates the phosphorylation-dependent degradation of beta-catenin. A protein phosphatase 2A (PP2A) regulatory subunit, B56, interacted with APC in the yeast two-hybrid system. Expression of B56 reduced the abundance of beta-catenin and inhibited transcription of beta-catenin target genes in mammalian cells and Xenopus embryo explants. The B56-dependent decrease in beta-catenin was blocked by oncogenic mutations in beta-catenin or APC, and by proteasome inhibitors. B56 may direct PP2A to dephosphorylate specific components of the APC-dependent signaling complex and thereby inhibit Wnt signaling.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Seeling, J M -- Miller, J R -- Gil, R -- Moon, R T -- White, R -- Virshup, D M -- 3P30CA42014/CA/NCI NIH HHS/ -- R01 CA71074/CA/NCI NIH HHS/ -- T32CA09602/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1999 Mar 26;283(5410):2089-91.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Oncological Sciences, Huntsman Cancer Institute, University of Utah, Salt Lake City, UT 84132, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10092233" target="_blank"〉PubMed〈/a〉
    Keywords: Adenomatous Polyposis Coli Protein ; Animals ; Calcium-Calmodulin-Dependent Protein Kinases/metabolism ; Cell Line ; Cysteine Endopeptidases/metabolism ; Cysteine Proteinase Inhibitors/pharmacology ; Cytoskeletal Proteins/genetics/*metabolism ; Down-Regulation ; Genes, Reporter ; Glycogen Synthase Kinase 3 ; Glycogen Synthase Kinases ; Humans ; Leupeptins/pharmacology ; Multienzyme Complexes/metabolism ; Mutation ; Phosphoprotein Phosphatases/chemistry/genetics/*metabolism ; Phosphorylation ; Proteasome Endopeptidase Complex ; Protein Phosphatase 2 ; Proto-Oncogene Proteins/*metabolism ; *Signal Transduction ; *Trans-Activators ; Transcriptional Activation ; Transfection ; Tumor Cells, Cultured ; Wnt Proteins ; Xenopus ; Xenopus Proteins ; *Zebrafish Proteins ; beta Catenin
    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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  • 7
    Publication Date: 2002-04-27
    Description: Reports of substantial evidence for genetic linkage of schizophrenia to chromosome 1q were evaluated by genotyping 16 DNA markers across 107 centimorgans of this chromosome in a multicenter sample of 779 informative schizophrenia pedigrees. No significant evidence was observed for such linkage, nor for heterogeneity in allele sharing among the eight individual samples. Separate analyses of European-origin families, recessive models of inheritance, and families with larger numbers of affected cases also failed to produce significant evidence for linkage. If schizophrenia susceptibility genes are present on chromosome 1q, their population-wide genetic effects are likely to be small.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Levinson, Douglas F -- Holmans, Peter A -- Laurent, Claudine -- Riley, Brien -- Pulver, Ann E -- Gejman, Pablo V -- Schwab, Sibylle G -- Williams, Nigel M -- Owen, Michael J -- Wildenauer, Dieter B -- Sanders, Alan R -- Nestadt, Gerald -- Mowry, Bryan J -- Wormley, Brandon -- Bauche, Stephanie -- Soubigou, Stephane -- Ribble, Robert -- Nertney, Deborah A -- Liang, Kung Yee -- Martinolich, Laura -- Maier, Wolfgang -- Norton, Nadine -- Williams, Hywel -- Albus, Margot -- Carpenter, Eric B -- DeMarchi, Nicola -- Ewen-White, Kelly R -- Walsh, Dermot -- Jay, Maurice -- Deleuze, Jean-Francois -- O'Neill, F Anthony -- Papadimitriou, George -- Weilbaecher, Ann -- Lerer, Bernard -- O'Donovan, Michael C -- Dikeos, Dimitris -- Silverman, Jeremy M -- Kendler, Kenneth S -- Mallet, Jacques -- Crowe, Raymond R -- Walters, Marilyn -- G9309834/Medical Research Council/United Kingdom -- G9810900/Medical Research Council/United Kingdom -- K24-MH64197/MH/NIMH NIH HHS/ -- KO2-01207/PHS HHS/ -- MH 41953/MH/NIMH NIH HHS/ -- MH 45390/MH/NIMH NIH HHS/ -- MH 52537/MH/NIMH NIH HHS/ -- MH61602/MH/NIMH NIH HHS/ -- R01-MH57314/MH/NIMH NIH HHS/ -- U01 MH46289/MH/NIMH NIH HHS/ -- U01 MH46318/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 2002 Apr 26;296(5568):739-41.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Psychiatry, University of Pennsylvania, Philadelphia, PA 19104, USA. dfl@mail.med.upenn.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11976456" target="_blank"〉PubMed〈/a〉
    Keywords: Africa ; Alleles ; Australia ; Canada ; Chromosomes, Human, Pair 1/*genetics ; Europe ; Female ; Genes, Recessive ; *Genetic Linkage ; *Genetic Predisposition to Disease ; Genotype ; Humans ; Lod Score ; Male ; Microsatellite Repeats ; Pedigree ; Schizophrenia/ethnology/*genetics ; United States
    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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  • 8
    Publication Date: 2002-06-29
    Description: Myeloperoxidase (MPO) is an abundant mammalian phagocyte hemoprotein thought to primarily mediate host defense reactions. Although its microbicidal functions are well established in vitro, humans deficient in MPO are not at unusual risk of infection. MPO was observed herein to modulate the vascular signaling and vasodilatory functions of nitric oxide (NO) during acute inflammation. After leukocyte degranulation, MPO localized in and around vascular endothelial cells in a rodent model of acute endotoxemia and impaired endothelium-dependent relaxant responses, to which MPO-deficient mice were resistant. Altered vascular responsiveness was due to catalytic consumption of NO by substrate radicals generated by MPO. Thus MPO can directly modulate vascular inflammatory responses by regulating NO bioavailability.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Eiserich, Jason P -- Baldus, Stephan -- Brennan, Marie-Luise -- Ma, Wenxin -- Zhang, Chunxiang -- Tousson, Albert -- Castro, Laura -- Lusis, Aldons J -- Nauseef, William M -- White, C Roger -- Freeman, Bruce A -- I01 BX000513/BX/BLRD VA/ -- R01 HL067930/HL/NHLBI NIH HHS/ -- R03 TW005682/TW/FIC NIH HHS/ -- New York, N.Y. -- Science. 2002 Jun 28;296(5577):2391-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Internal Medicine, Division of Nephrology, University of California, Davis, CA 95616, USA. jpeiserich@ucdavis.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12089442" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Aorta ; Catalysis ; Cattle ; Cells, Cultured ; Chromans/metabolism/pharmacology ; Coculture Techniques ; Cyclic GMP/metabolism ; Endothelium, Vascular/enzymology/*physiology ; Endotoxemia/enzymology ; Humans ; Hydrogen Peroxide/metabolism/pharmacology ; Inflammation/*enzymology/physiopathology ; Leukocytes/*enzymology ; Mice ; Mice, Inbred C57BL ; Muscle, Smooth, Vascular/metabolism ; Mutation ; Nitric Oxide/*metabolism ; Oxidation-Reduction ; Peroxidase/genetics/*metabolism ; Rats ; Rats, Sprague-Dawley ; Signal Transduction ; Transfection ; Tumor Cells, Cultured ; *Vasodilation
    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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  • 9
    Publication Date: 2000-09-08
    Description: Myotonic dystrophy (DM), the most common form of muscular dystrophy in adult humans, results from expansion of a CTG repeat in the 3' untranslated region of the DMPK gene. The mutant DMPK messenger RNA (mRNA) contains an expanded CUG repeat and is retained in the nucleus. We have expressed an untranslated CUG repeat in an unrelated mRNA in transgenic mice. Mice that expressed expanded CUG repeats developed myotonia and myopathy, whereas mice expressing a nonexpanded repeat did not. Thus, transcripts with expanded CUG repeats are sufficient to generate a DM phenotype. This result supports a role for RNA gain of function in disease pathogenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mankodi, A -- Logigian, E -- Callahan, L -- McClain, C -- White, R -- Henderson, D -- Krym, M -- Thornton, C A -- New York, N.Y. -- Science. 2000 Sep 8;289(5485):1769-73.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurology, School of Medicine and Dentistry, University of Rochester, Box 673, 601 Elmwood Avenue, Rochester, NY 14642, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10976074" target="_blank"〉PubMed〈/a〉
    Keywords: 3' Untranslated Regions ; Actins/genetics ; Action Potentials ; Animals ; Cell Nucleus/metabolism/pathology ; Disease Models, Animal ; Humans ; In Situ Hybridization, Fluorescence ; Mice ; Mice, Transgenic ; Muscle, Skeletal/metabolism/pathology/physiopathology ; Myotonic Dystrophy/*genetics/metabolism/pathology/physiopathology ; Myotonin-Protein Kinase ; Phenotype ; Protein-Serine-Threonine Kinases/genetics ; RNA Splicing ; RNA, Messenger/*genetics/metabolism ; Transgenes ; *Trinucleotide Repeat Expansion
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 10
    Publication Date: 2002-09-21
    Description: We report here the adoptive transfer, to patients with metastatic melanoma, of highly selected tumor-reactive T cells directed against overexpressed self-derived differentiation antigens after a nonmyeloablative conditioning regimen. This approach resulted in the persistent clonal repopulation of T cells in those cancer patients, with the transferred cells proliferating in vivo, displaying functional activity, and trafficking to tumor sites. This led to regression of the patients' metastatic melanoma as well as to the onset of autoimmune melanocyte destruction. This approach presents new possibilities for the treatment of patients with cancer as well as patients with human immunodeficiency virus-related acquired immunodeficiency syndrome and other infectious diseases.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1764179/" 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/PMC1764179/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dudley, Mark E -- Wunderlich, John R -- Robbins, Paul F -- Yang, James C -- Hwu, Patrick -- Schwartzentruber, Douglas J -- Topalian, Suzanne L -- Sherry, Richard -- Restifo, Nicholas P -- Hubicki, Amy M -- Robinson, Michael R -- Raffeld, Mark -- Duray, Paul -- Seipp, Claudia A -- Rogers-Freezer, Linda -- Morton, Kathleen E -- Mavroukakis, Sharon A -- White, Donald E -- Rosenberg, Steven A -- Z01 BC010763-01/Intramural NIH HHS/ -- Z99 CA999999/Intramural NIH HHS/ -- New York, N.Y. -- Science. 2002 Oct 25;298(5594):850-4. Epub 2002 Sep 19.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Surgery Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20902, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12242449" target="_blank"〉PubMed〈/a〉
    Keywords: Adolescent ; Adult ; Antigens, Neoplasm ; *Autoimmunity ; CD8-Positive T-Lymphocytes/immunology ; Clone Cells ; Cytokines/secretion ; Female ; HLA-A2 Antigen/immunology ; Histocompatibility Antigens Class I/immunology ; Histocompatibility Antigens Class II/immunology ; Humans ; *Immunotherapy, Adoptive ; Interleukin-2/therapeutic use ; Lymphocyte Count ; Lymphocyte Depletion ; Lymphocytes, Tumor-Infiltrating/*immunology ; MART-1 Antigen ; Male ; Melanocytes/immunology ; Melanoma/*immunology/pathology/secondary/*therapy ; Middle Aged ; Neoplasm Proteins/immunology ; Receptors, Antigen, T-Cell, alpha-beta/immunology ; T-Lymphocytes/*immunology ; Treatment Outcome
    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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