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  • Gene Expression Profiling  (2)
  • Female
  • Molecular Sequence Data
  • Nature Publishing Group (NPG)  (4)
  • 1
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    Genome sequence of the palaeopolyploid soybean (2010)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2010-01-16
    Description: Soybean (Glycine max) is one of the most important crop plants for seed protein and oil content, and for its capacity to fix atmospheric nitrogen through symbioses with soil-borne microorganisms. We sequenced the 1.1-gigabase genome by a whole-genome shotgun approach and integrated it with physical and high-density genetic maps to create a chromosome-scale draft sequence assembly. We predict 46,430 protein-coding genes, 70% more than Arabidopsis and similar to the poplar genome which, like soybean, is an ancient polyploid (palaeopolyploid). About 78% of the predicted genes occur in chromosome ends, which comprise less than one-half of the genome but account for nearly all of the genetic recombination. Genome duplications occurred at approximately 59 and 13 million years ago, resulting in a highly duplicated genome with nearly 75% of the genes present in multiple copies. The two duplication events were followed by gene diversification and loss, and numerous chromosome rearrangements. An accurate soybean genome sequence will facilitate the identification of the genetic basis of many soybean traits, and accelerate the creation of improved soybean varieties.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schmutz, Jeremy -- Cannon, Steven B -- Schlueter, Jessica -- Ma, Jianxin -- Mitros, Therese -- Nelson, William -- Hyten, David L -- Song, Qijian -- Thelen, Jay J -- Cheng, Jianlin -- Xu, Dong -- Hellsten, Uffe -- May, Gregory D -- Yu, Yeisoo -- Sakurai, Tetsuya -- Umezawa, Taishi -- Bhattacharyya, Madan K -- Sandhu, Devinder -- Valliyodan, Babu -- Lindquist, Erika -- Peto, Myron -- Grant, David -- Shu, Shengqiang -- Goodstein, David -- Barry, Kerrie -- Futrell-Griggs, Montona -- Abernathy, Brian -- Du, Jianchang -- Tian, Zhixi -- Zhu, Liucun -- Gill, Navdeep -- Joshi, Trupti -- Libault, Marc -- Sethuraman, Anand -- Zhang, Xue-Cheng -- Shinozaki, Kazuo -- Nguyen, Henry T -- Wing, Rod A -- Cregan, Perry -- Specht, James -- Grimwood, Jane -- Rokhsar, Dan -- Stacey, Gary -- Shoemaker, Randy C -- Jackson, Scott A -- England -- Nature. 2010 Jan 14;463(7278):178-83. doi: 10.1038/nature08670.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉HudsonAlpha Genome Sequencing Center, 601 Genome Way, Huntsville, Alabama 35806, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20075913" target="_blank"〉PubMed〈/a〉
    Keywords: Arabidopsis/genetics ; Breeding ; Chromosomes, Plant/genetics ; Evolution, Molecular ; Gene Duplication ; Genes, Duplicate/genetics ; Genes, Plant/genetics ; Genome, Plant/*genetics ; *Genomics ; Molecular Sequence Data ; Multigene Family/genetics ; Phylogeny ; Plant Root Nodulation/genetics ; *Polyploidy ; Quantitative Trait Loci/genetics ; Recombination, Genetic ; Repetitive Sequences, Nucleic Acid/genetics ; Soybean Oil/biosynthesis ; Soybeans/*genetics ; Synteny/genetics ; Transcription Factors/genetics
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 2
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    Interpreting cancer genomes using systematic host network perturbations by tumour virus proteins (2012)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2012-07-20
    Description: Genotypic differences greatly influence susceptibility and resistance to disease. Understanding genotype-phenotype relationships requires that phenotypes be viewed as manifestations of network properties, rather than simply as the result of individual genomic variations. Genome sequencing efforts have identified numerous germline mutations, and large numbers of somatic genomic alterations, associated with a predisposition to cancer. However, it remains difficult to distinguish background, or 'passenger', cancer mutations from causal, or 'driver', mutations in these data sets. Human viruses intrinsically depend on their host cell during the course of infection and can elicit pathological phenotypes similar to those arising from mutations. Here we test the hypothesis that genomic variations and tumour viruses may cause cancer through related mechanisms, by systematically examining host interactome and transcriptome network perturbations caused by DNA tumour virus proteins. The resulting integrated viral perturbation data reflects rewiring of the host cell networks, and highlights pathways, such as Notch signalling and apoptosis, that go awry in cancer. We show that systematic analyses of host targets of viral proteins can identify cancer genes with a success rate on a par with their identification through functional genomics and large-scale cataloguing of tumour mutations. Together, these complementary approaches increase the specificity of cancer gene identification. Combining systems-level studies of pathogen-encoded gene products with genomic approaches will facilitate the prioritization of cancer-causing driver genes to advance the understanding of the genetic basis of human cancer.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3408847/" 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/PMC3408847/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rozenblatt-Rosen, Orit -- Deo, Rahul C -- Padi, Megha -- Adelmant, Guillaume -- Calderwood, Michael A -- Rolland, Thomas -- Grace, Miranda -- Dricot, Amelie -- Askenazi, Manor -- Tavares, Maria -- Pevzner, Samuel J -- Abderazzaq, Fieda -- Byrdsong, Danielle -- Carvunis, Anne-Ruxandra -- Chen, Alyce A -- Cheng, Jingwei -- Correll, Mick -- Duarte, Melissa -- Fan, Changyu -- Feltkamp, Mariet C -- Ficarro, Scott B -- Franchi, Rachel -- Garg, Brijesh K -- Gulbahce, Natali -- Hao, Tong -- Holthaus, Amy M -- James, Robert -- Korkhin, Anna -- Litovchick, Larisa -- Mar, Jessica C -- Pak, Theodore R -- Rabello, Sabrina -- Rubio, Renee -- Shen, Yun -- Singh, Saurav -- Spangle, Jennifer M -- Tasan, Murat -- Wanamaker, Shelly -- Webber, James T -- Roecklein-Canfield, Jennifer -- Johannsen, Eric -- Barabasi, Albert-Laszlo -- Beroukhim, Rameen -- Kieff, Elliott -- Cusick, Michael E -- Hill, David E -- Munger, Karl -- Marto, Jarrod A -- Quackenbush, John -- Roth, Frederick P -- DeCaprio, James A -- Vidal, Marc -- F32 GM095284/GM/NIGMS NIH HHS/ -- F32GM095284/GM/NIGMS NIH HHS/ -- K08 CA122833/CA/NCI NIH HHS/ -- K08 HL098361/HL/NHLBI NIH HHS/ -- K08HL098361/HL/NHLBI NIH HHS/ -- K25 HG006031/HG/NHGRI NIH HHS/ -- K25HG006031/HG/NHGRI NIH HHS/ -- P01 CA050661/CA/NCI NIH HHS/ -- P01CA050661/CA/NCI NIH HHS/ -- P50 HG004233/HG/NHGRI NIH HHS/ -- P50HG004233/HG/NHGRI NIH HHS/ -- R01 CA047006/CA/NCI NIH HHS/ -- R01 CA063113/CA/NCI NIH HHS/ -- R01 CA066980/CA/NCI NIH HHS/ -- R01 CA081135/CA/NCI NIH HHS/ -- R01 CA085180/CA/NCI NIH HHS/ -- R01 CA093804/CA/NCI NIH HHS/ -- R01 CA131354/CA/NCI NIH HHS/ -- R01 HG001715/HG/NHGRI NIH HHS/ -- R01CA047006/CA/NCI NIH HHS/ -- R01CA063113/CA/NCI NIH HHS/ -- R01CA066980/CA/NCI NIH HHS/ -- R01CA081135/CA/NCI NIH HHS/ -- R01CA085180/CA/NCI NIH HHS/ -- R01CA093804/CA/NCI NIH HHS/ -- R01CA131354/CA/NCI NIH HHS/ -- R01HG001715/HG/NHGRI NIH HHS/ -- T32 HL007208/HL/NHLBI NIH HHS/ -- T32HL007208/HL/NHLBI NIH HHS/ -- U01 CA141583/CA/NCI NIH HHS/ -- U01CA141583/CA/NCI NIH HHS/ -- England -- Nature. 2012 Jul 26;487(7408):491-5. doi: 10.1038/nature11288.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Genomic Analysis of Network Perturbations Center of Excellence in Genomic Science, Dana-Farber Cancer Institute, Boston, Massachusetts 02215, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22810586" target="_blank"〉PubMed〈/a〉
    Keywords: Adenoviridae/genetics/metabolism/pathogenicity ; Gene Expression Profiling ; Gene Expression Regulation, Neoplastic ; Genes, Neoplasm/*genetics ; Genome, Human/*genetics ; Herpesvirus 4, Human/genetics/metabolism/pathogenicity ; *Host-Pathogen Interactions/genetics ; Humans ; Neoplasms/*genetics/*metabolism/pathology ; Oncogenic Viruses/genetics/metabolism/*pathogenicity ; Open Reading Frames/genetics ; Papillomaviridae/genetics/metabolism/pathogenicity ; Polyomavirus/genetics/metabolism/pathogenicity ; Receptors, Notch/metabolism ; Signal Transduction ; Two-Hybrid System Techniques ; Viral Proteins/genetics/*metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 3
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    The Cancer Cell Line Encyclopedia enables predictive modelling of anticancer drug sensitivity (2012)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2012-03-31
    Description: The systematic translation of cancer genomic data into knowledge of tumour biology and therapeutic possibilities remains challenging. Such efforts should be greatly aided by robust preclinical model systems that reflect the genomic diversity of human cancers and for which detailed genetic and pharmacological annotation is available. Here we describe the Cancer Cell Line Encyclopedia (CCLE): a compilation of gene expression, chromosomal copy number and massively parallel sequencing data from 947 human cancer cell lines. When coupled with pharmacological profiles for 24 anticancer drugs across 479 of the cell lines, this collection allowed identification of genetic, lineage, and gene-expression-based predictors of drug sensitivity. In addition to known predictors, we found that plasma cell lineage correlated with sensitivity to IGF1 receptor inhibitors; AHR expression was associated with MEK inhibitor efficacy in NRAS-mutant lines; and SLFN11 expression predicted sensitivity to topoisomerase inhibitors. Together, our results indicate that large, annotated cell-line collections may help to enable preclinical stratification schemata for anticancer agents. The generation of genetic predictions of drug response in the preclinical setting and their incorporation into cancer clinical trial design could speed the emergence of 'personalized' therapeutic regimens.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3320027/" 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/PMC3320027/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barretina, Jordi -- Caponigro, Giordano -- Stransky, Nicolas -- Venkatesan, Kavitha -- Margolin, Adam A -- Kim, Sungjoon -- Wilson, Christopher J -- Lehar, Joseph -- Kryukov, Gregory V -- Sonkin, Dmitriy -- Reddy, Anupama -- Liu, Manway -- Murray, Lauren -- Berger, Michael F -- Monahan, John E -- Morais, Paula -- Meltzer, Jodi -- Korejwa, Adam -- Jane-Valbuena, Judit -- Mapa, Felipa A -- Thibault, Joseph -- Bric-Furlong, Eva -- Raman, Pichai -- Shipway, Aaron -- Engels, Ingo H -- Cheng, Jill -- Yu, Guoying K -- Yu, Jianjun -- Aspesi, Peter Jr -- de Silva, Melanie -- Jagtap, Kalpana -- Jones, Michael D -- Wang, Li -- Hatton, Charles -- Palescandolo, Emanuele -- Gupta, Supriya -- Mahan, Scott -- Sougnez, Carrie -- Onofrio, Robert C -- Liefeld, Ted -- MacConaill, Laura -- Winckler, Wendy -- Reich, Michael -- Li, Nanxin -- Mesirov, Jill P -- Gabriel, Stacey B -- Getz, Gad -- Ardlie, Kristin -- Chan, Vivien -- Myer, Vic E -- Weber, Barbara L -- Porter, Jeff -- Warmuth, Markus -- Finan, Peter -- Harris, Jennifer L -- Meyerson, Matthew -- Golub, Todd R -- Morrissey, Michael P -- Sellers, William R -- Schlegel, Robert -- Garraway, Levi A -- DP2 OD002750/OD/NIH HHS/ -- DP2 OD002750-01/OD/NIH HHS/ -- R33 CA126674/CA/NCI NIH HHS/ -- R33 CA126674-04/CA/NCI NIH HHS/ -- R33 CA155554/CA/NCI NIH HHS/ -- R33 CA155554-02/CA/NCI NIH HHS/ -- England -- Nature. 2012 Mar 28;483(7391):603-7. doi: 10.1038/nature11003.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Broad Institute of Harvard and MIT, Cambridge, Massachusetts 02142, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22460905" target="_blank"〉PubMed〈/a〉
    Keywords: Antineoplastic Agents/pharmacology ; Cell Line, Tumor ; Cell Lineage ; Chromosomes, Human/genetics ; Clinical Trials as Topic/methods ; *Databases, Factual ; Drug Screening Assays, Antitumor/*methods ; *Encyclopedias as Topic ; Gene Expression Profiling ; Gene Expression Regulation, Neoplastic ; Genes, ras/genetics ; Genome, Human/genetics ; Genomics ; Humans ; Mitogen-Activated Protein Kinase Kinases/antagonists & inhibitors/metabolism ; *Models, Biological ; Neoplasms/*drug therapy/genetics/metabolism/*pathology ; Pharmacogenetics ; Plasma Cells/cytology/drug effects/metabolism ; Precision Medicine/methods ; Receptor, IGF Type 1/antagonists & inhibitors/metabolism ; Receptors, Aryl Hydrocarbon/genetics/metabolism ; Sequence Analysis, DNA ; Topoisomerase Inhibitors/pharmacology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 4
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    MicroRNA silencing for cancer therapy targeted to the tumour microenvironment (2014)
    Nature Publishing Group (NPG)
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    Publication Date: 2014-11-20
    Description: MicroRNAs are short non-coding RNAs expressed in different tissue and cell types that suppress the expression of target genes. As such, microRNAs are critical cogs in numerous biological processes, and dysregulated microRNA expression is correlated with many human diseases. Certain microRNAs, called oncomiRs, play a causal role in the onset and maintenance of cancer when overexpressed. Tumours that depend on these microRNAs are said to display oncomiR addiction. Some of the most effective anticancer therapies target oncogenes such as EGFR and HER2; similarly, inhibition of oncomiRs using antisense oligomers (that is, antimiRs) is an evolving therapeutic strategy. However, the in vivo efficacy of current antimiR technologies is hindered by physiological and cellular barriers to delivery into targeted cells. Here we introduce a novel antimiR delivery platform that targets the acidic tumour microenvironment, evades systemic clearance by the liver, and facilitates cell entry via a non-endocytic pathway. We find that the attachment of peptide nucleic acid antimiRs to a peptide with a low pH-induced transmembrane structure (pHLIP) produces a novel construct that could target the tumour microenvironment, transport antimiRs across plasma membranes under acidic conditions such as those found in solid tumours (pH approximately 6), and effectively inhibit the miR-155 oncomiR in a mouse model of lymphoma. This study introduces a new model for using antimiRs as anti-cancer drugs, which can have broad impacts on the field of targeted drug delivery.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4367962/" 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/PMC4367962/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cheng, Christopher J -- Bahal, Raman -- Babar, Imran A -- Pincus, Zachary -- Barrera, Francisco -- Liu, Connie -- Svoronos, Alexander -- Braddock, Demetrios T -- Glazer, Peter M -- Engelman, Donald M -- Saltzman, W Mark -- Slack, Frank J -- 2T32HL007974/HL/NHLBI NIH HHS/ -- F32 CA174247/CA/NCI NIH HHS/ -- F32CA174247/CA/NCI NIH HHS/ -- P30 CA016359/CA/NCI NIH HHS/ -- R00 AG042487/AG/NIA NIH HHS/ -- R01 CA131301/CA/NCI NIH HHS/ -- R01 CA148996/CA/NCI NIH HHS/ -- R01 CA149128/CA/NCI NIH HHS/ -- R01 EB000487/EB/NIBIB NIH HHS/ -- R01 ES005775/ES/NIEHS NIH HHS/ -- R01 GM073857/GM/NIGMS NIH HHS/ -- R01 HL085416/HL/NHLBI NIH HHS/ -- R01CA131301/CA/NCI NIH HHS/ -- R01CA148996/CA/NCI NIH HHS/ -- R01EB000487/EB/NIBIB NIH HHS/ -- R01ES005775/ES/NIEHS NIH HHS/ -- R01GM073857/GM/NIGMS NIH HHS/ -- R01HL085416/HL/NHLBI NIH HHS/ -- T32 GM007205/GM/NIGMS NIH HHS/ -- T32 HL007974/HL/NHLBI NIH HHS/ -- UL1 TR000142/TR/NCATS NIH HHS/ -- England -- Nature. 2015 Feb 5;518(7537):107-10. doi: 10.1038/nature13905. Epub 2014 Nov 17.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Department of Molecular, Cellular and Developmental Biology, Yale University, New Haven, Connecticut 06511, USA [2] Department of Biomedical Engineering, Yale University, New Haven, Connecticut 06511, USA [3] Department of Molecular Biophysics and Biochemistry, Yale University, New Haven, Connecticut 06511, USA. ; Department of Therapeutic Radiology, Yale University, New Haven, Connecticut 06511, USA. ; Department of Molecular, Cellular and Developmental Biology, Yale University, New Haven, Connecticut 06511, USA. ; Department of Molecular Biophysics and Biochemistry, Yale University, New Haven, Connecticut 06511, USA. ; Department of Pathology, Yale University, New Haven, Connecticut 06511, USA. ; Department of Biomedical Engineering, Yale University, New Haven, Connecticut 06511, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25409146" target="_blank"〉PubMed〈/a〉
    Keywords: Acids ; Animals ; Cell Membrane/metabolism ; Cell Membrane Permeability ; Disease Models, Animal ; *Drug Delivery Systems ; Female ; *Gene Expression Regulation, Neoplastic ; *Gene Silencing ; Hydrogen-Ion Concentration ; Lymphoma/*genetics/pathology/*therapy ; Male ; Mice ; MicroRNAs/*antagonists & inhibitors/genetics ; Molecular Targeted Therapy ; Nanoparticles/administration & dosage/chemistry ; Oncogenes/genetics ; Peptide Nucleic Acids/administration & dosage/chemistry/therapeutic use ; *Tumor Microenvironment/genetics
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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