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  • 1
    Publication Date: 2016-03-19
    Description: De Montjoye et al. (Reports, 30 January 2015, p. 536) claimed that most individuals can be reidentified from a deidentified transaction database and that anonymization mechanisms are not effective against reidentification. We demonstrate that anonymization can be performed by techniques well established in the literature.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sanchez, David -- Martinez, Sergio -- Domingo-Ferrer, Josep -- New York, N.Y. -- Science. 2016 Mar 18;351(6279):1274. doi: 10.1126/science.aad9295.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉United Nations Educational, Scientific, and Cultural Organization (UNESCO) Chair in Data Privacy, Department of Computer Engineering and Mathematics, Universitat Rovira i Virgili (URV), Avenue Paisos Catalans, 26, E-43007, Tarragona, Catalonia. david.sanchez@urv.cat. ; United Nations Educational, Scientific, and Cultural Organization (UNESCO) Chair in Data Privacy, Department of Computer Engineering and Mathematics, Universitat Rovira i Virgili (URV), Avenue Paisos Catalans, 26, E-43007, Tarragona, Catalonia.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26989243" target="_blank"〉PubMed〈/a〉
    Keywords: *Commerce ; *Data Collection ; Female ; Humans ; *Information Dissemination ; Male ; *Privacy
    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: 2014-06-12
    Description: Cutaneous melanoma is epidemiologically linked to ultraviolet radiation (UVR), but the molecular mechanisms by which UVR drives melanomagenesis remain unclear. The most common somatic mutation in melanoma is a V600E substitution in BRAF, which is an early event. To investigate how UVR accelerates oncogenic BRAF-driven melanomagenesis, we used a BRAF(V600E) mouse model. In mice expressing BRAF(V600E) in their melanocytes, a single dose of UVR that mimicked mild sunburn in humans induced clonal expansion of the melanocytes, and repeated doses of UVR increased melanoma burden. Here we show that sunscreen (UVA superior, UVB sun protection factor (SPF) 50) delayed the onset of UVR-driven melanoma, but only provided partial protection. The UVR-exposed tumours showed increased numbers of single nucleotide variants and we observed mutations (H39Y, S124F, R245C, R270C, C272G) in the Trp53 tumour suppressor in approximately 40% of cases. TP53 is an accepted UVR target in human non-melanoma skin cancer, but is not thought to have a major role in melanoma. However, we show that, in mice, mutant Trp53 accelerated BRAF(V600E)-driven melanomagenesis, and that TP53 mutations are linked to evidence of UVR-induced DNA damage in human melanoma. Thus, we provide mechanistic insight into epidemiological data linking UVR to acquired naevi in humans. Furthermore, we identify TP53/Trp53 as a UVR-target gene that cooperates with BRAF(V600E) to induce melanoma, providing molecular insight into how UVR accelerates melanomagenesis. Our study validates public health campaigns that promote sunscreen protection for individuals at risk of melanoma.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4112218/" 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/PMC4112218/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Viros, Amaya -- Sanchez-Laorden, Berta -- Pedersen, Malin -- Furney, Simon J -- Rae, Joel -- Hogan, Kate -- Ejiama, Sarah -- Girotti, Maria Romina -- Cook, Martin -- Dhomen, Nathalie -- Marais, Richard -- A12738/Cancer Research UK/United Kingdom -- A13540/Cancer Research UK/United Kingdom -- A17240/Cancer Research UK/United Kingdom -- A7091/Cancer Research UK/United Kingdom -- A7192/Cancer Research UK/United Kingdom -- C107/A10433/Cancer Research UK/United Kingdom -- C5759/A12328/Cancer Research UK/United Kingdom -- England -- Nature. 2014 Jul 24;511(7510):478-82. doi: 10.1038/nature13298. Epub 2014 Jun 11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Molecular Oncology Group, Cancer Research UK Manchester Institute, University of Manchester, Wilmslow Road, Manchester M20 4BX, UK [2]. ; 1] Signal Transduction Team, Institute of Cancer Research, 237 Fulham Road, London SW3 6JB, UK [2]. ; Signal Transduction Team, Institute of Cancer Research, 237 Fulham Road, London SW3 6JB, UK. ; Molecular Oncology Group, Cancer Research UK Manchester Institute, University of Manchester, Wilmslow Road, Manchester M20 4BX, UK. ; 1] Molecular Oncology Group, Cancer Research UK Manchester Institute, University of Manchester, Wilmslow Road, Manchester M20 4BX, UK [2] Histopathology, Royal Surrey County Hospital, Egerton Road, Guildford GU2 7XX, UK. ; 1] Molecular Oncology Group, Cancer Research UK Manchester Institute, University of Manchester, Wilmslow Road, Manchester M20 4BX, UK [2] Signal Transduction Team, Institute of Cancer Research, 237 Fulham Road, London SW3 6JB, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24919155" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Cell Transformation, Neoplastic/*genetics/*radiation effects ; DNA Damage/genetics ; Disease Models, Animal ; Female ; Humans ; Melanocytes/metabolism/pathology/radiation effects ; Melanoma/etiology/*genetics/metabolism/*pathology ; Mice ; Mice, Inbred C57BL ; Mutagenesis/genetics/*radiation effects ; Mutation/genetics/radiation effects ; Nevus/etiology/genetics/metabolism/pathology ; Proto-Oncogene Proteins B-raf/*genetics/metabolism ; Skin Neoplasms/etiology/genetics/metabolism/pathology ; Sunburn/complications/etiology/genetics ; Sunscreening Agents/pharmacology ; Tumor Suppressor Protein p53/*genetics/metabolism ; Ultraviolet Rays/*adverse effects
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 3
    Publication Date: 2014-07-22
    Description: Myeloproliferative neoplasms (MPNs) are diseases caused by mutations in the haematopoietic stem cell (HSC) compartment. Most MPN patients have a common acquired mutation of Janus kinase 2 (JAK2) gene in HSCs that renders this kinase constitutively active, leading to uncontrolled cell expansion. The bone marrow microenvironment might contribute to the clinical outcomes of this common event. We previously showed that bone marrow nestin(+) mesenchymal stem cells (MSCs) innervated by sympathetic nerve fibres regulate normal HSCs. Here we demonstrate that abrogation of this regulatory circuit is essential for MPN pathogenesis. Sympathetic nerve fibres, supporting Schwann cells and nestin(+) MSCs are consistently reduced in the bone marrow of MPN patients and mice expressing the human JAK2(V617F) mutation in HSCs. Unexpectedly, MSC reduction is not due to differentiation but is caused by bone marrow neural damage and Schwann cell death triggered by interleukin-1beta produced by mutant HSCs. In turn, in vivo depletion of nestin(+) cells or their production of CXCL12 expanded mutant HSC number and accelerated MPN progression. In contrast, administration of neuroprotective or sympathomimetic drugs prevented mutant HSC expansion. Treatment with beta3-adrenergic agonists that restored the sympathetic regulation of nestin(+) MSCs prevented the loss of these cells and blocked MPN progression by indirectly reducing the number of leukaemic stem cells. Our results demonstrate that mutant-HSC-driven niche damage critically contributes to disease manifestation in MPN and identify niche-forming MSCs and their neural regulation as promising therapeutic targets.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Arranz, Lorena -- Sanchez-Aguilera, Abel -- Martin-Perez, Daniel -- Isern, Joan -- Langa, Xavier -- Tzankov, Alexandar -- Lundberg, Pontus -- Muntion, Sandra -- Tzeng, Yi-Shiuan -- Lai, Dar-Ming -- Schwaller, Jurg -- Skoda, Radek C -- Mendez-Ferrer, Simon -- Howard Hughes Medical Institute/ -- England -- Nature. 2014 Aug 7;512(7512):78-81. doi: 10.1038/nature13383. Epub 2014 Jun 22.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Stem Cell Niche Pathophysiology Group, Centro Nacional de Investigaciones Cardiovasculares (CNIC), 28029 Madrid, Spain. ; University Hospital Basel, CH-4031 Basel, Switzerland. ; Department of Haematology, IBSAL-Hospital Universitario de Salamanca, 37007 Salamanca, Spain. ; National Taiwan University, Taipei 10002, Taiwan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25043017" target="_blank"〉PubMed〈/a〉
    Keywords: Adrenergic beta-3 Receptor Agonists/pharmacology/therapeutic use ; Animals ; Apoptosis/drug effects ; Disease Progression ; Female ; Hematopoietic Stem Cells/drug effects/*pathology ; Humans ; Interleukin-1beta/metabolism ; Janus Kinase 2/genetics ; Mesenchymal Stromal Cells/drug effects/pathology ; Mice ; Myeloproliferative Disorders/drug therapy/*pathology ; Neoplasms/drug therapy/*pathology ; Neoplastic Stem Cells/drug effects/pathology ; Nerve Fibers/drug effects/*pathology ; Nestin/metabolism ; Neuroprotective Agents/pharmacology/therapeutic use ; Receptors, Adrenergic, beta-3/metabolism ; Schwann Cells/drug effects/pathology ; *Stem Cell Niche ; Sympathetic Nervous System/drug effects/*pathology/physiopathology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 4
    Publication Date: 2015-05-15
    Description: The tumour microenvironment may contribute to tumorigenesis owing to mechanical forces such as fibrotic stiffness or mechanical pressure caused by the expansion of hyper-proliferative cells. Here we explore the contribution of the mechanical pressure exerted by tumour growth onto non-tumorous adjacent epithelium. In the early stage of mouse colon tumour development in the Notch(+)Apc(+/1638N) mouse model, we observed mechanistic pressure stress in the non-tumorous epithelial cells caused by hyper-proliferative adjacent crypts overexpressing active Notch, which is associated with increased Ret and beta-catenin signalling. We thus developed a method that allows the delivery of a defined mechanical pressure in vivo, by subcutaneously inserting a magnet close to the mouse colon. The implanted magnet generated a magnetic force on ultra-magnetic liposomes, stabilized in the mesenchymal cells of the connective tissue surrounding colonic crypts after intravenous injection. The magnetically induced pressure quantitatively mimicked the endogenous early tumour growth stress in the order of 1,200 Pa, without affecting tissue stiffness, as monitored by ultrasound strain imaging and shear wave elastography. The exertion of pressure mimicking that of tumour growth led to rapid Ret activation and downstream phosphorylation of beta-catenin on Tyr654, imparing its interaction with the E-cadherin in adherens junctions, and which was followed by beta-catenin nuclear translocation after 15 days. As a consequence, increased expression of beta-catenin-target genes was observed at 1 month, together with crypt enlargement accompanying the formation of early tumorous aberrant crypt foci. Mechanical activation of the tumorigenic beta-catenin pathway suggests unexplored modes of tumour propagation based on mechanical signalling pathways in healthy epithelial cells surrounding the tumour, which may contribute to tumour heterogeneity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fernandez-Sanchez, Maria Elena -- Barbier, Sandrine -- Whitehead, Joanne -- Bealle, Gaelle -- Michel, Aude -- Latorre-Ossa, Heldmuth -- Rey, Colette -- Fouassier, Laura -- Claperon, Audrey -- Brulle, Laura -- Girard, Elodie -- Servant, Nicolas -- Rio-Frio, Thomas -- Marie, Helene -- Lesieur, Sylviane -- Housset, Chantal -- Gennisson, Jean-Luc -- Tanter, Mickael -- Menager, Christine -- Fre, Silvia -- Robine, Sylvie -- Farge, Emmanuel -- England -- Nature. 2015 Jul 2;523(7558):92-5. doi: 10.1038/nature14329. Epub 2015 May 11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institut Curie, Centre de Recherche, PSL Research University, CNRS UMR 168, Physicochimie Curie Mechanics and Genetics of Embryonic and Tumour Development, INSERM, Fondation Pierre-Gilles de Gennes, F-75005 Paris, France. ; UPMC, Sorbonne Universites, Laboratoire PHENIX Physico-chimie des Electrolytes et Nanosystemes Interfaciaux, CNRS UMR 8234, F-75005 Paris, France. ; Langevin Institut, Waves and Images ESPCI ParisTech, PSL Research University, CNRS UMR7587, Inserm U979. F-75005 Paris, France. ; Sorbonne Universites, UPMC and INSERM, UMR-S 938, CDR Saint-Antoine, F-75012 Paris, France. ; CNRS UMR3666/INSERM U1143, Endocytic Trafficking and Therapeutic Delivery, Institut Curie, Centre de Recherche, F-75005 Paris, France. ; Bioinformatic platform, U900, Institut Curie, MINES ParisTech, F-75005 Paris, France. ; Next-generation sequencing platform, Institut Curie, F-75005 Paris, France. ; CNRS UMR 8612, Laboratoire Physico-Chimie des Systemes Polyphases, Institut Galien Paris-Sud, LabEx LERMIT, Faculte de Pharmacie, Universite Paris-Sud, 92 296 Chatenay-Malabry, France. ; CNRS UMR 3215/INSERM U934, Unite de Genetique et Biologie du Developpement, Notch Signaling in Stem Cells and Tumors, Institut Curie, Centre de Recherche, F-75005 Paris, France. ; CNRS UMR144, Compartimentation et dynamique cellulaires, Morphogenesis and Cell Signalling Institut Curie, Centre de Recherche, F-75005 Paris, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25970250" target="_blank"〉PubMed〈/a〉
    Keywords: Active Transport, Cell Nucleus ; Animals ; Carcinogenesis/*pathology ; Colonic Neoplasms/*physiopathology ; Epithelial Cells/cytology/pathology ; Female ; Gene Expression Regulation, Neoplastic ; Magnets ; Male ; Metal Nanoparticles ; Mice ; Mice, Inbred C57BL ; Phosphorylation ; *Pressure ; Proto-Oncogene Proteins c-ret/metabolism ; Receptors, Notch/genetics/metabolism ; Signal Transduction ; *Tumor Microenvironment ; beta Catenin/*genetics/metabolism
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    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 5
    Publication Date: 2014-06-06
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sanchez, Irma -- Dynlacht, Brian D -- England -- Nature. 2014 Jun 5;510(7503):40-2. doi: 10.1038/510040a.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉New York University School of Medicine, New York, New York 10016, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24899299" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calmodulin-Binding Proteins/*deficiency/*genetics ; Cilia/*genetics/*physiology ; Female ; Male ; MicroRNAs/*genetics ; Morphogenesis/*genetics
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 6
    Publication Date: 2015-03-13
    Description: After stimulation, dendritic cells (DCs) mature and migrate to draining lymph nodes to induce immune responses. As such, autologous DCs generated ex vivo have been pulsed with tumour antigens and injected back into patients as immunotherapy. While DC vaccines have shown limited promise in the treatment of patients with advanced cancers including glioblastoma, the factors dictating DC vaccine efficacy remain poorly understood. Here we show that pre-conditioning the vaccine site with a potent recall antigen such as tetanus/diphtheria (Td) toxoid can significantly improve the lymph node homing and efficacy of tumour-antigen-specific DCs. To assess the effect of vaccine site pre-conditioning in humans, we randomized patients with glioblastoma to pre-conditioning with either mature DCs or Td unilaterally before bilateral vaccination with DCs pulsed with Cytomegalovirus phosphoprotein 65 (pp65) RNA. We and other laboratories have shown that pp65 is expressed in more than 90% of glioblastoma specimens but not in surrounding normal brain, providing an unparalleled opportunity to subvert this viral protein as a tumour-specific target. Patients given Td had enhanced DC migration bilaterally and significantly improved survival. In mice, Td pre-conditioning also enhanced bilateral DC migration and suppressed tumour growth in a manner dependent on the chemokine CCL3. Our clinical studies and corroborating investigations in mice suggest that pre-conditioning with a potent recall antigen may represent a viable strategy to improve anti-tumour immunotherapy.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4510871/" 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/PMC4510871/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mitchell, Duane A -- Batich, Kristen A -- Gunn, Michael D -- Huang, Min-Nung -- Sanchez-Perez, Luis -- Nair, Smita K -- Congdon, Kendra L -- Reap, Elizabeth A -- Archer, Gary E -- Desjardins, Annick -- Friedman, Allan H -- Friedman, Henry S -- Herndon, James E 2nd -- Coan, April -- McLendon, Roger E -- Reardon, David A -- Vredenburgh, James J -- Bigner, Darell D -- Sampson, John H -- 1UL2 RR024128-01/RR/NCRR NIH HHS/ -- P01 CA154291/CA/NCI NIH HHS/ -- P01-CA154291-01A1/CA/NCI NIH HHS/ -- P50 CA108786/CA/NCI NIH HHS/ -- P50 NS020023/NS/NINDS NIH HHS/ -- P50-CA108786/CA/NCI NIH HHS/ -- P50-NS20023/NS/NINDS NIH HHS/ -- R01 CA134844/CA/NCI NIH HHS/ -- R01 CA177476/CA/NCI NIH HHS/ -- R01 NS067037/NS/NINDS NIH HHS/ -- R01-CA134844/CA/NCI NIH HHS/ -- R01-CA177476-01/CA/NCI NIH HHS/ -- R01-NS067037/NS/NINDS NIH HHS/ -- T32 AI052077/AI/NIAID NIH HHS/ -- T32 GM007171/GM/NIGMS NIH HHS/ -- England -- Nature. 2015 Mar 19;519(7543):366-9. doi: 10.1038/nature14320. Epub 2015 Mar 11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Preston Robert Tisch Brain Tumor Center, Duke University Medical Center, Durham, North Carolina 27710, USA [2] Division of Neurosurgery, Department of Surgery, Duke University Medical Center, Durham, North Carolina 27710, USA [3] Department of Pathology, Duke University Medical Center, Durham, North Carolina 27710, USA. ; 1] Division of Neurosurgery, Department of Surgery, Duke University Medical Center, Durham, North Carolina 27710, USA [2] Department of Pathology, Duke University Medical Center, Durham, North Carolina 27710, USA. ; 1] Division of Cardiology, Department of Medicine, Duke University Medical Center, Durham, North Carolina 27710, USA [2] Department of Immunology, Duke University Medical Center, Durham, North Carolina 27710, USA. ; Department of Immunology, Duke University Medical Center, Durham, North Carolina 27710, USA. ; Division of Neurosurgery, Department of Surgery, Duke University Medical Center, Durham, North Carolina 27710, USA. ; Division of Surgical Sciences, Department of Surgery, Duke University Medical Center, Durham, North Carolina 27710, USA. ; 1] Preston Robert Tisch Brain Tumor Center, Duke University Medical Center, Durham, North Carolina 27710, USA [2] Division of Neurosurgery, Department of Surgery, Duke University Medical Center, Durham, North Carolina 27710, USA. ; Department of Biostatistics and Bioinformatics, Duke University Medical Center, Durham, North Carolina 27710, USA. ; 1] Preston Robert Tisch Brain Tumor Center, Duke University Medical Center, Durham, North Carolina 27710, USA [2] Department of Pathology, Duke University Medical Center, Durham, North Carolina 27710, USA. ; 1] Preston Robert Tisch Brain Tumor Center, Duke University Medical Center, Durham, North Carolina 27710, USA [2] Division of Neurosurgery, Department of Surgery, Duke University Medical Center, Durham, North Carolina 27710, USA [3] Department of Pathology, Duke University Medical Center, Durham, North Carolina 27710, USA [4] Department of Immunology, Duke University Medical Center, Durham, North Carolina 27710, USA [5] Department of Radiation Oncology, Duke University Medical Center, Durham, North Carolina 27710, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25762141" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, Neoplasm/immunology ; CD4-Positive T-Lymphocytes/drug effects/immunology ; Cancer Vaccines/administration & dosage/*immunology/therapeutic use ; Cell Movement/drug effects ; Chemokine CCL3/*immunology ; Dendritic Cells/cytology/*drug effects/immunology ; Female ; Glioblastoma/drug therapy/*immunology/pathology/*therapy ; Humans ; Immunotherapy/methods ; Lymph Nodes/cytology/drug effects/immunology ; Mice ; Mice, Inbred C57BL ; Phosphoproteins/chemistry/genetics/immunology ; Substrate Specificity ; Survival Rate ; Tetanus Toxoid/*administration & dosage/*pharmacology/therapeutic use ; Treatment Outcome ; Viral Matrix Proteins/chemistry/genetics/immunology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 7
    Publication Date: 1995-03-03
    Description: Cell cycle checkpoints enhance genetic fidelity by causing arrest at specific stages of the cell cycle when previous events have not been completed. The tumor suppressor p53 has been implicated in a G1 checkpoint. To investigate whether p53 also participates in a mitotic checkpoint, cultured fibroblasts from p53-deficient mouse embryos were exposed to spindle inhibitors. The fibroblasts underwent multiple rounds of DNA synthesis without completing chromosome segregation, thus forming tetraploid and octaploid cells. Deficiency of p53 was also associated with the development of tetraploidy in vivo. These results suggest that murine p53 is a component of a spindle checkpoint that ensures the maintenance of diploidy.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cross, S M -- Sanchez, C A -- Morgan, C A -- Schimke, M K -- Ramel, S -- Idzerda, R L -- Raskind, W H -- Reid, B J -- R01CA55814/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1995 Mar 3;267(5202):1353-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, University of Washington, Seattle 98195.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7871434" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Cycle ; Cells, Cultured ; DNA/biosynthesis ; Demecolcine/pharmacology ; Diploidy ; Female ; Genes, p53 ; Male ; Mice ; *Mitosis ; Nocodazole/pharmacology ; Ploidies ; Spindle Apparatus/*physiology ; Tumor Suppressor Protein p53/*physiology
    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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  • 8
    Publication Date: 2005-10-01
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Grant, Robert M -- Buchbinder, Susan -- Cates, Willard Jr -- Clarke, Edith -- Coates, Thomas -- Cohen, Myron S -- Delaney, Martin -- Flores, Guiselly -- Goicochea, Pedro -- Gonsalves, Gregg -- Harrington, Mark -- Lama, Javier R -- MacQueen, Kathleen M -- Moore, John P -- Peterson, Leigh -- Sanchez, Jorge -- Thompson, Melanie -- Wainberg, Mark A -- New York, N.Y. -- Science. 2005 Sep 30;309(5744):2170-1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Gladstone Institute of Virology and Immunology, San Francisco, CA, USA. rgrant@itsa.ucsf.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16195446" target="_blank"〉PubMed〈/a〉
    Keywords: Adenine/adverse effects/*analogs & derivatives/economics/therapeutic use ; Africa ; Anti-HIV Agents/adverse effects/economics/*therapeutic use ; Asia ; Consumer Participation ; *Controlled Clinical Trials as Topic/standards ; Counseling ; Developing Countries ; Drug Costs ; Female ; HIV Infections/*prevention & control ; Health Services Accessibility ; Humans ; Latin America ; Male ; Organophosphonates/adverse effects/economics/*therapeutic use ; Patient Selection ; Tenofovir
    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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  • 9
    Publication Date: 2006-11-04
    Description: Reduction of core body temperature has been proposed to contribute to the increased life span and the antiaging effects conferred by calorie restriction (CR). Validation of this hypothesis has been difficult in homeotherms, primarily due to a lack of experimental models. We report that transgenic mice engineered to overexpress the uncoupling protein 2 in hypocretin neurons (Hcrt-UCP2) have elevated hypothalamic temperature. The effects of local temperature elevation on the central thermostat resulted in a 0.3 degrees to 0.5 degrees C reduction of the core body temperature. Fed ad libitum, Hcrt-UCP2 transgenic mice had the same caloric intake as their wild-type littermates but had increased energy efficiency and a greater median life span (12% increase in males; 20% increase in females). Thus, modest, sustained reduction of core body temperature prolonged life span independent of altered diet or CR.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Conti, Bruno -- Sanchez-Alavez, Manuel -- Winsky-Sommerer, Raphaelle -- Morale, Maria Concetta -- Lucero, Jacinta -- Brownell, Sara -- Fabre, Veronique -- Huitron-Resendiz, Salvador -- Henriksen, Steven -- Zorrilla, Eric P -- de Lecea, Luis -- Bartfai, Tamas -- MH58543/MH/NIMH NIH HHS/ -- NS043501/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2006 Nov 3;314(5800):825-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Harold L. Dorris Neurological Research Center, Scripps Research Institute, La Jolla, CA 92037, USA. bconti@scripps.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17082459" target="_blank"〉PubMed〈/a〉
    Keywords: Aging ; Animals ; *Body Temperature ; Body Temperature Regulation ; Body Weight ; Circadian Rhythm ; Drinking ; Eating ; Energy Metabolism ; Female ; Hypothalamic Area, Lateral/cytology/metabolism ; Intracellular Signaling Peptides and Proteins/metabolism ; Ion Channels/genetics/physiology ; *Longevity ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Mitochondrial Proteins/genetics/physiology ; Neurons/metabolism ; Neuropeptides/metabolism ; Orexins ; Preoptic Area/cytology/*physiology ; Thermogenesis
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 10
    Publication Date: 2010-07-03
    Description: Residents of the Tibetan Plateau show heritable adaptations to extreme altitude. We sequenced 50 exomes of ethnic Tibetans, encompassing coding sequences of 92% of human genes, with an average coverage of 18x per individual. Genes showing population-specific allele frequency changes, which represent strong candidates for altitude adaptation, were identified. The strongest signal of natural selection came from endothelial Per-Arnt-Sim (PAS) domain protein 1 (EPAS1), a transcription factor involved in response to hypoxia. One single-nucleotide polymorphism (SNP) at EPAS1 shows a 78% frequency difference between Tibetan and Han samples, representing the fastest allele frequency change observed at any human gene to date. This SNP's association with erythrocyte abundance supports the role of EPAS1 in adaptation to hypoxia. Thus, a population genomic survey has revealed a functionally important locus in genetic adaptation to high altitude.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3711608/" 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/PMC3711608/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yi, Xin -- Liang, Yu -- Huerta-Sanchez, Emilia -- Jin, Xin -- Cuo, Zha Xi Ping -- Pool, John E -- Xu, Xun -- Jiang, Hui -- Vinckenbosch, Nicolas -- Korneliussen, Thorfinn Sand -- Zheng, Hancheng -- Liu, Tao -- He, Weiming -- Li, Kui -- Luo, Ruibang -- Nie, Xifang -- Wu, Honglong -- Zhao, Meiru -- Cao, Hongzhi -- Zou, Jing -- Shan, Ying -- Li, Shuzheng -- Yang, Qi -- Asan -- Ni, Peixiang -- Tian, Geng -- Xu, Junming -- Liu, Xiao -- Jiang, Tao -- Wu, Renhua -- Zhou, Guangyu -- Tang, Meifang -- Qin, Junjie -- Wang, Tong -- Feng, Shuijian -- Li, Guohong -- Huasang -- Luosang, Jiangbai -- Wang, Wei -- Chen, Fang -- Wang, Yading -- Zheng, Xiaoguang -- Li, Zhuo -- Bianba, Zhuoma -- Yang, Ge -- Wang, Xinping -- Tang, Shuhui -- Gao, Guoyi -- Chen, Yong -- Luo, Zhen -- Gusang, Lamu -- Cao, Zheng -- Zhang, Qinghui -- Ouyang, Weihan -- Ren, Xiaoli -- Liang, Huiqing -- Zheng, Huisong -- Huang, Yebo -- Li, Jingxiang -- Bolund, Lars -- Kristiansen, Karsten -- Li, Yingrui -- Zhang, Yong -- Zhang, Xiuqing -- Li, Ruiqiang -- Li, Songgang -- Yang, Huanming -- Nielsen, Rasmus -- Wang, Jun -- Wang, Jian -- R01 HG003229/HG/NHGRI NIH HHS/ -- R01 MH084695/MH/NIMH NIH HHS/ -- R01HG003229/HG/NHGRI NIH HHS/ -- R01MHG084695/PHS HHS/ -- New York, N.Y. -- Science. 2010 Jul 2;329(5987):75-8. doi: 10.1126/science.1190371.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉BGI-Shenzhen, Shenzhen 518083, China.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20595611" target="_blank"〉PubMed〈/a〉
    Keywords: Acclimatization/*genetics ; *Altitude ; Asian Continental Ancestry Group/genetics ; Basic Helix-Loop-Helix Transcription Factors/*genetics/physiology ; Bayes Theorem ; China ; Erythrocyte Count ; Ethnic Groups/genetics ; *Exons ; Female ; Gene Frequency ; Genetic Association Studies ; *Genome, Human ; Hemoglobins/analysis ; Humans ; Male ; Oxygen/blood ; Polymorphism, Single Nucleotide ; *Selection, Genetic ; Sequence Analysis, DNA ; Tibet
    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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