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  • 1
    Publication Date: 2002-03-02
    Description: Development of the body plan is controlled by large networks of regulatory genes. A gene regulatory network that controls the specification of endoderm and mesoderm in the sea urchin embryo is summarized here. The network was derived from large-scale perturbation analyses, in combination with computational methodologies, genomic data, cis-regulatory analysis, and molecular embryology. The network contains over 40 genes at present, and each node can be directly verified at the DNA sequence level by cis-regulatory analysis. Its architecture reveals specific and general aspects of development, such as how given cells generate their ordained fates in the embryo and why the process moves inexorably forward in developmental time.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Davidson, Eric H -- Rast, Jonathan P -- Oliveri, Paola -- Ransick, Andrew -- Calestani, Cristina -- Yuh, Chiou-Hwa -- Minokawa, Takuya -- Amore, Gabriele -- Hinman, Veronica -- Arenas-Mena, Cesar -- Otim, Ochan -- Brown, C Titus -- Livi, Carolina B -- Lee, Pei Yun -- Revilla, Roger -- Rust, Alistair G -- Pan, Zheng jun -- Schilstra, Maria J -- Clarke, Peter J C -- Arnone, Maria I -- Rowen, Lee -- Cameron, R Andrew -- McClay, David R -- Hood, Leroy -- Bolouri, Hamid -- GM-61005/GM/NIGMS NIH HHS/ -- HD-37105/HD/NICHD NIH HHS/ -- RR-06591/RR/NCRR NIH HHS/ -- RR-15044/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 2002 Mar 1;295(5560):1669-78.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Biology, California Institute of Technology, Pasadena, CA 91125, USA. davidson@caltech.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11872831" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Lineage ; Computational Biology ; Embryonic Development ; Endoderm/cytology/*physiology ; Gene Expression Profiling ; *Gene Expression Regulation, Developmental ; Genes, Regulator ; *Genome ; Mesoderm/cytology/*physiology ; Models, Biological ; Models, Genetic ; Morphogenesis ; Regulatory Sequences, Nucleic Acid ; Sea Urchins/*embryology/*genetics ; Stem Cells/physiology ; Systems Theory
    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: 2009-02-07
    Description: Great-appendage arthropods, characterized by a highly modified anterior limb, were previously unknown after the Middle Cambrian. One fossil from the Lower Devonian Hunsruck Slate, Germany, extends the stratigraphic range of these arthropods by approximately 100 million years. Schinderhannes bartelsi shows an unusual combination of anomalocaridid and euarthropod characters, including a highly specialized swimming appendage. A cladistic analysis indicates that the new taxon is basal to crown-group euarthropods and that the great-appendage arthropods are paraphyletic. This new fossil shows that features of the anomalocaridids, including the multisegmented raptorial appendage and circular plated mouth, persisted long after the initial radiation of the euarthropods.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kuhl, Gabriele -- Briggs, Derek E G -- Rust, Jes -- New York, N.Y. -- Science. 2009 Feb 6;323(5915):771-3. doi: 10.1126/science.1166586.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Palaeontology, Steinmann Institute, University of Bonn, Nussallee 8, 53115 Bonn, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19197061" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Arthropods/*anatomy & histology/*classification ; Extremities/anatomy & histology ; *Fossils ; Germany ; Mouth/anatomy & histology ; Phylogeny
    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: 2012-09-18
    Description: Antiviral responses must be tightly regulated to defend rapidly against infection while minimizing inflammatory damage. Type 1 interferons (IFN-I) are crucial mediators of antiviral responses and their transcription is regulated by a variety of transcription factors; principal among these is the family of interferon regulatory factors (IRFs). The IRF gene regulatory networks are complex and contain multiple feedback loops. The tools of systems biology are well suited to elucidate the complex interactions that give rise to precise coordination of the interferon response. Here we have used an unbiased systems approach to predict that a member of the forkhead family of transcription factors, FOXO3, is a negative regulator of a subset of antiviral genes. This prediction was validated using macrophages isolated from Foxo3-null mice. Genome-wide location analysis combined with gene deletion studies identified the Irf7 gene as a critical target of FOXO3. FOXO3 was identified as a negative regulator of Irf7 transcription and we have further demonstrated that FOXO3, IRF7 and IFN-I form a coherent feed-forward regulatory circuit. Our data suggest that the FOXO3-IRF7 regulatory circuit represents a novel mechanism for establishing the requisite set points in the interferon pathway that balances the beneficial effects and deleterious sequelae of the antiviral response.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3556990/" 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/PMC3556990/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Litvak, Vladimir -- Ratushny, Alexander V -- Lampano, Aaron E -- Schmitz, Frank -- Huang, Albert C -- Raman, Ayush -- Rust, Alistair G -- Bergthaler, Andreas -- Aitchison, John D -- Aderem, Alan -- HHSN272200700038C/AI/NIAID NIH HHS/ -- HHSN272200700038C/PHS HHS/ -- HHSN272200800058C/AI/NIAID NIH HHS/ -- HSN272200800058C/PHS HHS/ -- R01 AI025032/AI/NIAID NIH HHS/ -- R01 AI032972/AI/NIAID NIH HHS/ -- R01AI025032/AI/NIAID NIH HHS/ -- R01AI032972/AI/NIAID NIH HHS/ -- U19 AI100627/AI/NIAID NIH HHS/ -- U54 GM103511/GM/NIGMS NIH HHS/ -- U54 RR022220/RR/NCRR NIH HHS/ -- U54GM103511/GM/NIGMS NIH HHS/ -- England -- Nature. 2012 Oct 18;490(7420):421-5. doi: 10.1038/nature11428. Epub 2012 Sep 16.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Seattle Biomedical Research Institute, Seattle, Washington 98109, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22982991" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Female ; Forkhead Transcription Factors/deficiency/genetics/*metabolism ; Gene Deletion ; Gene Expression Regulation/*immunology ; Inflammation/genetics/*immunology/*pathology ; Interferon Regulatory Factor-7/deficiency/genetics/*metabolism ; Interferon Type I/immunology ; Lung/immunology/pathology/virology ; Macrophages/immunology ; Mice ; Mice, Inbred C57BL ; Reproducibility of Results ; Vesiculovirus/*immunology
    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: 2013-02-22
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hornschemeyer, Thomas -- Haug, Joachim T -- Bethoux, Olivier -- Beutel, Rolf G -- Charbonnier, Sylvain -- Hegna, Thomas A -- Koch, Markus -- Rust, Jes -- Wedmann, Sonja -- Bradler, Sven -- Willmann, Rainer -- England -- Nature. 2013 Feb 21;494(7437):E3-4; discussion E4-5. doi: 10.1038/nature11887.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Johann-Friedrich-Blumenbach-Institute of Zoology and Anthropology, Georg-August-University Gottingen, 37073 Gottingen, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23426326" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biological Evolution ; *Fossils ; Insects/*anatomy & histology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 5
    Publication Date: 2011-01-21
    Description: The genetics of renal cancer is dominated by inactivation of the VHL tumour suppressor gene in clear cell carcinoma (ccRCC), the commonest histological subtype. A recent large-scale screen of approximately 3,500 genes by PCR-based exon re-sequencing identified several new cancer genes in ccRCC including UTX (also known as KDM6A), JARID1C (also known as KDM5C) and SETD2 (ref. 2). These genes encode enzymes that demethylate (UTX, JARID1C) or methylate (SETD2) key lysine residues of histone H3. Modification of the methylation state of these lysine residues of histone H3 regulates chromatin structure and is implicated in transcriptional control. However, together these mutations are present in fewer than 15% of ccRCC, suggesting the existence of additional, currently unidentified cancer genes. Here, we have sequenced the protein coding exome in a series of primary ccRCC and report the identification of the SWI/SNF chromatin remodelling complex gene PBRM1 (ref. 4) as a second major ccRCC cancer gene, with truncating mutations in 41% (92/227) of cases. These data further elucidate the somatic genetic architecture of ccRCC and emphasize the marked contribution of aberrant chromatin biology.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3030920/" 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/PMC3030920/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Varela, Ignacio -- Tarpey, Patrick -- Raine, Keiran -- Huang, Dachuan -- Ong, Choon Kiat -- Stephens, Philip -- Davies, Helen -- Jones, David -- Lin, Meng-Lay -- Teague, Jon -- Bignell, Graham -- Butler, Adam -- Cho, Juok -- Dalgliesh, Gillian L -- Galappaththige, Danushka -- Greenman, Chris -- Hardy, Claire -- Jia, Mingming -- Latimer, Calli -- Lau, King Wai -- Marshall, John -- McLaren, Stuart -- Menzies, Andrew -- Mudie, Laura -- Stebbings, Lucy -- Largaespada, David A -- Wessels, L F A -- Richard, Stephane -- Kahnoski, Richard J -- Anema, John -- Tuveson, David A -- Perez-Mancera, Pedro A -- Mustonen, Ville -- Fischer, Andrej -- Adams, David J -- Rust, Alistair -- Chan-on, Waraporn -- Subimerb, Chutima -- Dykema, Karl -- Furge, Kyle -- Campbell, Peter J -- Teh, Bin Tean -- Stratton, Michael R -- Futreal, P Andrew -- 077012/Wellcome Trust/United Kingdom -- 077012/Z/05/Z/Wellcome Trust/United Kingdom -- 088340/Wellcome Trust/United Kingdom -- 093867/Wellcome Trust/United Kingdom -- R01 CA113636/CA/NCI NIH HHS/ -- R01 CA134759/CA/NCI NIH HHS/ -- Cancer Research UK/United Kingdom -- England -- Nature. 2011 Jan 27;469(7331):539-42. doi: 10.1038/nature09639. Epub 2011 Jan 19.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cancer Genome Project, Wellcome Trust Sanger Institute, Hinxton CB10 1SA, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21248752" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Carcinoma, Renal Cell/*genetics ; Cell Line, Tumor ; Disease Models, Animal ; Gene Expression Regulation ; Gene Knockdown Techniques ; Humans ; Kidney Neoplasms/*genetics ; Mice ; Mutation/*genetics ; Nuclear Proteins/*genetics/*metabolism ; Pancreatic Neoplasms/genetics ; Transcription Factors/*genetics/*metabolism
    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: 2012-10-30
    Description: Pancreatic cancer is a highly lethal malignancy with few effective therapies. We performed exome sequencing and copy number analysis to define genomic aberrations in a prospectively accrued clinical cohort (n = 142) of early (stage I and II) sporadic pancreatic ductal adenocarcinoma. Detailed analysis of 99 informative tumours identified substantial heterogeneity with 2,016 non-silent mutations and 1,628 copy-number variations. We define 16 significantly mutated genes, reaffirming known mutations (KRAS, TP53, CDKN2A, SMAD4, MLL3, TGFBR2, ARID1A and SF3B1), and uncover novel mutated genes including additional genes involved in chromatin modification (EPC1 and ARID2), DNA damage repair (ATM) and other mechanisms (ZIM2, MAP2K4, NALCN, SLC16A4 and MAGEA6). Integrative analysis with in vitro functional data and animal models provided supportive evidence for potential roles for these genetic aberrations in carcinogenesis. Pathway-based analysis of recurrently mutated genes recapitulated clustering in core signalling pathways in pancreatic ductal adenocarcinoma, and identified new mutated genes in each pathway. We also identified frequent and diverse somatic aberrations in genes described traditionally as embryonic regulators of axon guidance, particularly SLIT/ROBO signalling, which was also evident in murine Sleeping Beauty transposon-mediated somatic mutagenesis models of pancreatic cancer, providing further supportive evidence for the potential involvement of axon guidance genes in pancreatic carcinogenesis.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3530898/" 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/PMC3530898/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Biankin, Andrew V -- Waddell, Nicola -- Kassahn, Karin S -- Gingras, Marie-Claude -- Muthuswamy, Lakshmi B -- Johns, Amber L -- Miller, David K -- Wilson, Peter J -- Patch, Ann-Marie -- Wu, Jianmin -- Chang, David K -- Cowley, Mark J -- Gardiner, Brooke B -- Song, Sarah -- Harliwong, Ivon -- Idrisoglu, Senel -- Nourse, Craig -- Nourbakhsh, Ehsan -- Manning, Suzanne -- Wani, Shivangi -- Gongora, Milena -- Pajic, Marina -- Scarlett, Christopher J -- Gill, Anthony J -- Pinho, Andreia V -- Rooman, Ilse -- Anderson, Matthew -- Holmes, Oliver -- Leonard, Conrad -- Taylor, Darrin -- Wood, Scott -- Xu, Qinying -- Nones, Katia -- Fink, J Lynn -- Christ, Angelika -- Bruxner, Tim -- Cloonan, Nicole -- Kolle, Gabriel -- Newell, Felicity -- Pinese, Mark -- Mead, R Scott -- Humphris, Jeremy L -- Kaplan, Warren -- Jones, Marc D -- Colvin, Emily K -- Nagrial, Adnan M -- Humphrey, Emily S -- Chou, Angela -- Chin, Venessa T -- Chantrill, Lorraine A -- Mawson, Amanda -- Samra, Jaswinder S -- Kench, James G -- Lovell, Jessica A -- Daly, Roger J -- Merrett, Neil D -- Toon, Christopher -- Epari, Krishna -- Nguyen, Nam Q -- Barbour, Andrew -- Zeps, Nikolajs -- Australian Pancreatic Cancer Genome Initiative -- Kakkar, Nipun -- Zhao, Fengmei -- Wu, Yuan Qing -- Wang, Min -- Muzny, Donna M -- Fisher, William E -- Brunicardi, F Charles -- Hodges, Sally E -- Reid, Jeffrey G -- Drummond, Jennifer -- Chang, Kyle -- Han, Yi -- Lewis, Lora R -- Dinh, Huyen -- Buhay, Christian J -- Beck, Timothy -- Timms, Lee -- Sam, Michelle -- Begley, Kimberly -- Brown, Andrew -- Pai, Deepa -- Panchal, Ami -- Buchner, Nicholas -- De Borja, Richard -- Denroche, Robert E -- Yung, Christina K -- Serra, Stefano -- Onetto, Nicole -- Mukhopadhyay, Debabrata -- Tsao, Ming-Sound -- Shaw, Patricia A -- Petersen, Gloria M -- Gallinger, Steven -- Hruban, Ralph H -- Maitra, Anirban -- Iacobuzio-Donahue, Christine A -- Schulick, Richard D -- Wolfgang, Christopher L -- Morgan, Richard A -- Lawlor, Rita T -- Capelli, Paola -- Corbo, Vincenzo -- Scardoni, Maria -- Tortora, Giampaolo -- Tempero, Margaret A -- Mann, Karen M -- Jenkins, Nancy A -- Perez-Mancera, Pedro A -- Adams, David J -- Largaespada, David A -- Wessels, Lodewyk F A -- Rust, Alistair G -- Stein, Lincoln D -- Tuveson, David A -- Copeland, Neal G -- Musgrove, Elizabeth A -- Scarpa, Aldo -- Eshleman, James R -- Hudson, Thomas J -- Sutherland, Robert L -- Wheeler, David A -- Pearson, John V -- McPherson, John D -- Gibbs, Richard A -- Grimmond, Sean M -- 13031/Cancer Research UK/United Kingdom -- 2P50CA101955/CA/NCI NIH HHS/ -- P01CA134292/CA/NCI NIH HHS/ -- P50 CA101955/CA/NCI NIH HHS/ -- P50 CA102701/CA/NCI NIH HHS/ -- P50CA062924/CA/NCI NIH HHS/ -- R01 CA097075/CA/NCI NIH HHS/ -- R01 CA97075/CA/NCI NIH HHS/ -- U54 HG003273/HG/NHGRI NIH HHS/ -- Cancer Research UK/United Kingdom -- Wellcome Trust/United Kingdom -- England -- Nature. 2012 Nov 15;491(7424):399-405. doi: 10.1038/nature11547. Epub 2012 Oct 24.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Kinghorn Cancer Centre, 370 Victoria Street, Darlinghurst, Sydney, New South Wales 2010, Australia.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23103869" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axons/*metabolism ; Carcinoma, Pancreatic Ductal/*genetics/*pathology ; Gene Dosage ; Gene Expression Regulation, Neoplastic ; Genome/*genetics ; Humans ; Kaplan-Meier Estimate ; Mice ; Mutation ; Pancreatic Neoplasms/*genetics/*pathology ; Proteins/genetics ; Signal Transduction
    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: 2014-11-05
    Description: Next-generation sequencing of human tumours has refined our understanding of the mutational processes operative in cancer initiation and progression, yet major questions remain regarding the factors that induce driver mutations and the processes that shape mutation selection during tumorigenesis. Here we performed whole-exome sequencing on adenomas from three mouse models of non-small-cell lung cancer, which were induced either by exposure to carcinogens (methyl-nitrosourea (MNU) and urethane) or by genetic activation of Kras (Kras(LA2)). Although the MNU-induced tumours carried exactly the same initiating mutation in Kras as seen in the Kras(LA2) model (G12D), MNU tumours had an average of 192 non-synonymous, somatic single-nucleotide variants, compared with only six in tumours from the Kras(LA2) model. By contrast, the Kras(LA2) tumours exhibited a significantly higher level of aneuploidy and copy number alterations compared with the carcinogen-induced tumours, suggesting that carcinogen-induced and genetically engineered models lead to tumour development through different routes. The wild-type allele of Kras has been shown to act as a tumour suppressor in mouse models of non-small-cell lung cancer. We demonstrate that urethane-induced tumours from wild-type mice carry mostly (94%) Kras Q61R mutations, whereas those from Kras heterozygous animals carry mostly (92%) Kras Q61L mutations, indicating a major role for germline Kras status in mutation selection during initiation. The exome-wide mutation spectra in carcinogen-induced tumours overwhelmingly display signatures of the initiating carcinogen, while adenocarcinomas acquire additional C 〉 T mutations at CpG sites. These data provide a basis for understanding results from human tumour genome sequencing, which has identified two broad categories of tumours based on the relative frequency of single-nucleotide variations and copy number alterations, and underline the importance of carcinogen models for understanding the complex mutation spectra seen in human cancers.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4304785/" 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/PMC4304785/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Westcott, Peter M K -- Halliwill, Kyle D -- To, Minh D -- Rashid, Mamunur -- Rust, Alistair G -- Keane, Thomas M -- Delrosario, Reyno -- Jen, Kuang-Yu -- Gurley, Kay E -- Kemp, Christopher J -- Fredlund, Erik -- Quigley, David A -- Adams, David J -- Balmain, Allan -- 082356/Wellcome Trust/United Kingdom -- 13031/Cancer Research UK/United Kingdom -- A12401/Cancer Research UK/United Kingdom -- A13031/Cancer Research UK/United Kingdom -- A14356/Cancer Research UK/United Kingdom -- F31 CA180669/CA/NCI NIH HHS/ -- F31 CA180715/CA/NCI NIH HHS/ -- R01 CA111834/CA/NCI NIH HHS/ -- R01 CA184510/CA/NCI NIH HHS/ -- T32 GM007175/GM/NIGMS NIH HHS/ -- T32GM007175/GM/NIGMS NIH HHS/ -- U01 CA084244/CA/NCI NIH HHS/ -- U01 CA141455/CA/NCI NIH HHS/ -- U01 CA176287/CA/NCI NIH HHS/ -- U01 CA84244/CA/NCI NIH HHS/ -- UO1 CA176287/CA/NCI NIH HHS/ -- Cancer Research UK/United Kingdom -- Wellcome Trust/United Kingdom -- England -- Nature. 2015 Jan 22;517(7535):489-92. doi: 10.1038/nature13898. Epub 2014 Nov 2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Helen Diller Family Comprehensive Cancer Center, University of California San Francisco, San Francisco, California 94158, USA [2] Department of Bioengineering and Therapeutic Sciences, University of California San Francisco, San Francisco, California 94158, USA. ; Helen Diller Family Comprehensive Cancer Center, University of California San Francisco, San Francisco, California 94158, USA. ; Experimental Cancer Genetics, Wellcome Trust Sanger Institute, Hinxton, Cambridge CB10 1HH, UK. ; Department of Pathology, University of California San Francisco, San Francisco, California 94143, USA. ; Fred Hutchinson Cancer Research Center, Seattle, Washington 98109, USA. ; Science for Life Laboratory, Department of Oncology-Pathology, Karolinska Institute, Stockholm 171 21, Sweden. ; 1] Helen Diller Family Comprehensive Cancer Center, University of California San Francisco, San Francisco, California 94158, USA [2] Department of Biochemistry and Biophysics, University of California San Francisco, San Francisco, California 94158, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25363767" target="_blank"〉PubMed〈/a〉
    Keywords: Adenocarcinoma/chemically induced/genetics ; Animals ; Carcinogens/toxicity ; Carcinoma, Non-Small-Cell Lung/chemically induced/genetics ; Cell Transformation, Neoplastic/*chemically induced/*genetics ; DNA Copy Number Variations/genetics ; Disease Progression ; Female ; Genes, ras/*genetics ; Genomic Instability/genetics ; Germ-Line Mutation/genetics ; Humans ; Lung Neoplasms/*chemically induced/*genetics ; Male ; Methylnitrosourea/toxicity ; Mice ; Models, Genetic ; Mutation/*genetics ; Oncogene Protein p21(ras)/*genetics ; Point Mutation/genetics ; Proto-Oncogene Proteins p21(ras)/*genetics ; Urethane/toxicity
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    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 8
    Publication Date: 2012-06-16
    Description: Pancreatic ductal adenocarcinoma (PDA) remains a lethal malignancy despite much progress concerning its molecular characterization. PDA tumours harbour four signature somatic mutations in addition to numerous lower frequency genetic events of uncertain significance. Here we use Sleeping Beauty (SB) transposon-mediated insertional mutagenesis in a mouse model of pancreatic ductal preneoplasia to identify genes that cooperate with oncogenic Kras(G12D) to accelerate tumorigenesis and promote progression. Our screen revealed new candidate genes for PDA and confirmed the importance of many genes and pathways previously implicated in human PDA. The most commonly mutated gene was the X-linked deubiquitinase Usp9x, which was inactivated in over 50% of the tumours. Although previous work had attributed a pro-survival role to USP9X in human neoplasia, we found instead that loss of Usp9x enhances transformation and protects pancreatic cancer cells from anoikis. Clinically, low USP9X protein and messenger RNA expression in PDA correlates with poor survival after surgery, and USP9X levels are inversely associated with metastatic burden in advanced disease. Furthermore, chromatin modulation with trichostatin A or 5-aza-2'-deoxycytidine elevates USP9X expression in human PDA cell lines, indicating a clinical approach for certain patients. The conditional deletion of Usp9x cooperated with Kras(G12D) to accelerate pancreatic tumorigenesis in mice, validating their genetic interaction. We propose that USP9X is a major tumour suppressor gene with prognostic and therapeutic relevance in PDA.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3376394/" 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/PMC3376394/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Perez-Mancera, Pedro A -- Rust, Alistair G -- van der Weyden, Louise -- Kristiansen, Glen -- Li, Allen -- Sarver, Aaron L -- Silverstein, Kevin A T -- Grutzmann, Robert -- Aust, Daniela -- Rummele, Petra -- Knosel, Thomas -- Herd, Colin -- Stemple, Derek L -- Kettleborough, Ross -- Brosnan, Jacqueline A -- Li, Ang -- Morgan, Richard -- Knight, Spencer -- Yu, Jun -- Stegeman, Shane -- Collier, Lara S -- ten Hoeve, Jelle J -- de Ridder, Jeroen -- Klein, Alison P -- Goggins, Michael -- Hruban, Ralph H -- Chang, David K -- Biankin, Andrew V -- Grimmond, Sean M -- Australian Pancreatic Cancer Genome Initiative -- Wessels, Lodewyk F A -- Wood, Stephen A -- Iacobuzio-Donahue, Christine A -- Pilarsky, Christian -- Largaespada, David A -- Adams, David J -- Tuveson, David A -- 13031/Cancer Research UK/United Kingdom -- 2P50CA101955/CA/NCI NIH HHS/ -- CA106610/CA/NCI NIH HHS/ -- CA122183/CA/NCI NIH HHS/ -- CA128920/CA/NCI NIH HHS/ -- CA62924/CA/NCI NIH HHS/ -- K01 CA122183/CA/NCI NIH HHS/ -- K01 CA122183-05/CA/NCI NIH HHS/ -- P50 CA101955/CA/NCI NIH HHS/ -- P50CA62924/CA/NCI NIH HHS/ -- Cancer Research UK/United Kingdom -- Wellcome Trust/United Kingdom -- England -- Nature. 2012 Apr 29;486(7402):266-70. doi: 10.1038/nature11114.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Li Ka Shing Centre, Cambridge Research Institute, Cancer Research UK, Cambridge CB2 0RE, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22699621" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anoikis/genetics ; Carcinoma, Pancreatic Ductal/*enzymology/genetics/pathology ; Cell Line, Tumor ; Disease Models, Animal ; Endopeptidases ; Gene Expression Regulation, Neoplastic ; Gene Knockdown Techniques ; Humans ; Mice ; Mice, Inbred C57BL ; Pancreatic Neoplasms/*enzymology/genetics/pathology ; U937 Cells ; Ubiquitin Thiolesterase/*genetics/*metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 9
    Publication Date: 2014-11-08
    Description: Insects are the most speciose group of animals, but the phylogenetic relationships of many major lineages remain unresolved. We inferred the phylogeny of insects from 1478 protein-coding genes. Phylogenomic analyses of nucleotide and amino acid sequences, with site-specific nucleotide or domain-specific amino acid substitution models, produced statistically robust and congruent results resolving previously controversial phylogenetic relations hips. We dated the origin of insects to the Early Ordovician [~479 million years ago (Ma)], of insect flight to the Early Devonian (~406 Ma), of major extant lineages to the Mississippian (~345 Ma), and the major diversification of holometabolous insects to the Early Cretaceous. Our phylogenomic study provides a comprehensive reliable scaffold for future comparative analyses of evolutionary innovations among insects.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Misof, Bernhard -- Liu, Shanlin -- Meusemann, Karen -- Peters, Ralph S -- Donath, Alexander -- Mayer, Christoph -- Frandsen, Paul B -- Ware, Jessica -- Flouri, Tomas -- Beutel, Rolf G -- Niehuis, Oliver -- Petersen, Malte -- Izquierdo-Carrasco, Fernando -- Wappler, Torsten -- Rust, Jes -- Aberer, Andre J -- Aspock, Ulrike -- Aspock, Horst -- Bartel, Daniela -- Blanke, Alexander -- Berger, Simon -- Bohm, Alexander -- Buckley, Thomas R -- Calcott, Brett -- Chen, Junqing -- Friedrich, Frank -- Fukui, Makiko -- Fujita, Mari -- Greve, Carola -- Grobe, Peter -- Gu, Shengchang -- Huang, Ying -- Jermiin, Lars S -- Kawahara, Akito Y -- Krogmann, Lars -- Kubiak, Martin -- Lanfear, Robert -- Letsch, Harald -- Li, Yiyuan -- Li, Zhenyu -- Li, Jiguang -- Lu, Haorong -- Machida, Ryuichiro -- Mashimo, Yuta -- Kapli, Pashalia -- McKenna, Duane D -- Meng, Guanliang -- Nakagaki, Yasutaka -- Navarrete-Heredia, Jose Luis -- Ott, Michael -- Ou, Yanxiang -- Pass, Gunther -- Podsiadlowski, Lars -- Pohl, Hans -- von Reumont, Bjorn M -- Schutte, Kai -- Sekiya, Kaoru -- Shimizu, Shota -- Slipinski, Adam -- Stamatakis, Alexandros -- Song, Wenhui -- Su, Xu -- Szucsich, Nikolaus U -- Tan, Meihua -- Tan, Xuemei -- Tang, Min -- Tang, Jingbo -- Timelthaler, Gerald -- Tomizuka, Shigekazu -- Trautwein, Michelle -- Tong, Xiaoli -- Uchifune, Toshiki -- Walzl, Manfred G -- Wiegmann, Brian M -- Wilbrandt, Jeanne -- Wipfler, Benjamin -- Wong, Thomas K F -- Wu, Qiong -- Wu, Gengxiong -- Xie, Yinlong -- Yang, Shenzhou -- Yang, Qing -- Yeates, David K -- Yoshizawa, Kazunori -- Zhang, Qing -- Zhang, Rui -- Zhang, Wenwei -- Zhang, Yunhui -- Zhao, Jing -- Zhou, Chengran -- Zhou, Lili -- Ziesmann, Tanja -- Zou, Shijie -- Li, Yingrui -- Xu, Xun -- Zhang, Yong -- Yang, Huanming -- Wang, Jian -- Wang, Jun -- Kjer, Karl M -- Zhou, Xin -- New York, N.Y. -- Science. 2014 Nov 7;346(6210):763-7. doi: 10.1126/science.1257570. Epub 2014 Nov 6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Zoologisches Forschungsmuseum Alexander Koenig (ZFMK)/Zentrum fur Molekulare Biodiversitatsforschung (ZMB), Bonn, Germany. xinzhou@genomics.cn b.misof.zfmk@uni-bonn.de kjer@aesop.rutgers.edu wangj@genomics.cn. ; China National GeneBank, BGI-Shenzhen, China. BGI-Shenzhen, China. ; Zoologisches Forschungsmuseum Alexander Koenig (ZFMK)/Zentrum fur Molekulare Biodiversitatsforschung (ZMB), Bonn, Germany. Australian National Insect Collection, Commonwealth Scientific and Industrial Research Organization (Australia) (CSIRO), National Research Collections Australia, Canberra, ACT, Australia. ; Abteilung Arthropoda, Zoologisches Forschungsmuseum Alexander Koenig (ZFMK), Bonn, Germany. ; Zoologisches Forschungsmuseum Alexander Koenig (ZFMK)/Zentrum fur Molekulare Biodiversitatsforschung (ZMB), Bonn, Germany. ; Department of Entomology, Rutgers University, New Brunswick, NJ 08854, USA. ; Department of Biological Sciences, Rutgers University, Newark, NJ 08854, USA. ; Scientific Computing, Heidelberg Institute for Theoretical Studies (HITS), Heidelberg, Germany. ; Institut fur Spezielle Zoologie und Evolutionsbiologie mit Phyletischem Museum Jena, FSU Jena, Germany. ; Steinmann-Institut, Bereich Palaontologie, Universitat Bonn, Germany. ; 2. Zoologische Abteilung (Insekten), Naturhistorisches Museum Wien, Vienna, Austria. Department of Integrative Zoology, Universitat Wien, Vienna, Austria. ; Institut fur Spezifische Prophylaxe und Tropenmedizin, Medizinische Parasitologie, Medizinische Universitat Wien (MUW), Vienna, Austria. ; Department of Integrative Zoology, Universitat Wien, Vienna, Austria. ; Zoologisches Forschungsmuseum Alexander Koenig (ZFMK)/Zentrum fur Molekulare Biodiversitatsforschung (ZMB), Bonn, Germany. Sugadaira Montane Research Center/Hexapod Comparative Embryology Laboratory, University of Tsukuba, Japan. ; Manaaki Whenua Landcare Research, Auckland, New Zealand. ; Center for Advanced Modeling, Emergency Medicine Department, Johns Hopkins University, Baltimore, MD 21209, USA. ; BGI-Shenzhen, China. ; Biozentrum Grindel und Zoologisches Museum, Universitat Hamburg, Hamburg, Germany. ; Evolutionary Morphology Laboratory, Graduate School of Science and Engineering, Ehime University, Japan. ; Sugadaira Montane Research Center/Hexapod Comparative Embryology Laboratory, University of Tsukuba, Japan. ; Land and Water Flagship, CSIRO, Canberra, ACT, Australia. ; Florida Museum of Natural History, University of Florida, Gainesville, FL 32611, USA. ; Entomology, Staatliches Museum fur Naturkunde Stuttgart (SMNS), Germany. ; Ecology Evolution and Genetics, Research School of Biology, Australian National University, Canberra, ACT, Australia. National Evolutionary Synthesis Center, Durham, NC 27705, USA. Department of Biological Sciences, Macquarie University, Sydney, Australia. ; Department fur Botanik und Biodiversitatsforschung, Universitat Wien, Vienna, Austria. ; Scientific Computing, Heidelberg Institute for Theoretical Studies (HITS), Heidelberg, Germany. Natural History Museum of Crete, University of Crete, Post Office Box 2208, Gr-71409, Iraklio, and Biology Department, University of Crete, Iraklio, Crete, Greece. ; Department of Biological Sciences and Feinstone Center for Genomic Research, University of Memphis, Memphis, TN 38152, USA. ; Centro Universitario de Ciencias Biologicas y Agropecuarias, Centro de Estudios en Zoologia, Universidad de Guadalajara, Zapopan, Jalisco, Mexico. ; Leibniz Supercomputing Centre of the Bavarian Academy of Sciences and Humanities, Garching, Germany. ; Institute of Evolutionary Biology and Ecology, Zoology and Evolutionary Biology, University of Bonn, Bonn, Germany. ; Department of Life Sciences, The Natural History Museum London, London, UK. ; Abteilung Entomologie, Biozentrum Grindel und Zoologisches Museum, Universitat Hamburg, Hamburg, Germany. ; Australian National Insect Collection, Commonwealth Scientific and Industrial Research Organization (Australia) (CSIRO), National Research Collections Australia, Canberra, ACT, Australia. ; Scientific Computing, Heidelberg Institute for Theoretical Studies (HITS), Heidelberg, Germany. Fakultat fur Informatik, Karlsruher Institut fur Technologie, Karlsruhe, Germany. ; California Academy of Sciences, San Francisco, CA 94118, USA. ; Department of Entomology, College of Natural Resources and Environment, South China Agricultural University, China. ; Sugadaira Montane Research Center/Hexapod Comparative Embryology Laboratory, University of Tsukuba, Japan. Yokosuka City Museum, Yokosuka, Kanagawa, Japan. ; Department of Entomology, North Carolina State University, Raleigh, NC 27695, USA. ; Systematic Entomology, Hokkaido University, Sapporo, Japan. ; BGI-Shenzhen, China. Department of Biology, University of Copenhagen, Copenhagen, Denmark. Princess Al Jawhara Center of Excellence in the Research of Hereditary Disorders, King Abdulaziz University, Jeddah, Saudi Arabia. Macau University of Science and Technology, Avenida Wai Long, Taipa, Macau, China. Department of Medicine, University of Hong Kong, Hong Kong. xinzhou@genomics.cn b.misof.zfmk@uni-bonn.de kjer@aesop.rutgers.edu wangj@genomics.cn. ; Department of Ecology, Evolution, and Natural Resources, Rutgers University, New Brunswick, NJ 08854, USA. xinzhou@genomics.cn b.misof.zfmk@uni-bonn.de kjer@aesop.rutgers.edu wangj@genomics.cn. ; China National GeneBank, BGI-Shenzhen, China. BGI-Shenzhen, China. xinzhou@genomics.cn b.misof.zfmk@uni-bonn.de kjer@aesop.rutgers.edu wangj@genomics.cn.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25378627" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Genetic Code ; Genome, Insect ; Genomics ; Insect Proteins/*classification/genetics ; Insects/*classification/genetics ; *Phylogeny ; Time Factors
    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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  • 10
    Publication Date: 2015-08-01
    Description: Tong et al. comment on the accuracy of the dating analysis presented in our work on the phylogeny of insects and provide a reanalysis of our data. They replace log-normal priors with uniform priors and add a "roachoid" fossil as a calibration point. Although the reanalysis provides an interesting alternative viewpoint, we maintain that our choices were appropriate.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kjer, K M -- Ware, J L -- Rust, J -- Wappler, T -- Lanfear, R -- Jermiin, L S -- Zhou, X -- Aspock, H -- Aspock, U -- Beutel, R G -- Blanke, A -- Donath, A -- Flouri, T -- Frandsen, P B -- Kapli, P -- Kawahara, A Y -- Letsch, H -- Mayer, C -- McKenna, D D -- Meusemann, K -- Niehuis, O -- Peters, R S -- Wiegmann, B M -- Yeates, D K -- von Reumont, B M -- Stamatakis, A -- Misof, B -- New York, N.Y. -- Science. 2015 Jul 31;349(6247):487. doi: 10.1126/science.aaa7136.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉University of California, Davis, CA, USA. ; Rutgers University, New Brunswick, NJ, USA. ; Universitat Bonn, Germany. ; Macquarie University, Sydney, Australia. ; Commonwealth Scientific and Industrial Research Organization, Canberra, ACT, Australia. ; China National GeneBank, BGI-Shenzhen, China. BGI-Shenzhen, China. ; Universitat Wien, Vienna, Austria. ; Universitat Wien, Vienna, Austria. Naturhistorisches Museum Wien, Vienna, Austria. ; Phyletischem Museum Jena, Friedrich-Schiller-Universitat Jena, Germany. ; University of Tsukuba, Japan. ; Universitat Bonn, Germany. Zoologisches Forschungsmuseum Alexander Koenig (ZFMK), Bonn, Germany. ; Heidelberg Institute for Theoretical Studies (HITS), Heidelberg, Germany. ; Rutgers University, New Brunswick, NJ, USA. Smithsonian Institution, Washington, DC, USA. ; University of Florida, Gainesville, FL, USA. ; University of Memphis, Memphis, TN, USA. ; Commonwealth Scientific and Industrial Research Organization, Canberra, ACT, Australia. Zoologisches Forschungsmuseum Alexander Koenig (ZFMK), Bonn, Germany. ; Zoologisches Forschungsmuseum Alexander Koenig (ZFMK), Bonn, Germany. Arizona State University, Tempe, AZ, USA. ; North Carolina State University, Raleigh, NC, USA. ; Zoologisches Forschungsmuseum Alexander Koenig (ZFMK), Bonn, Germany. Natural History Museum London, London, UK. ; Zoologisches Forschungsmuseum Alexander Koenig (ZFMK), Bonn, Germany. bmisof@uni-bonn.de.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26228138" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Insect Proteins/*classification ; Insects/*classification ; *Phylogeny
    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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