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  • 1
    Publication Date: 2012-03-01
    Description: : High-throughput technologies can identify genes whose expression profiles correlate with specific phenotypes; however, placing these genes into a biological context remains challenging. To help address this issue, we developed nested Expression Analysis Systematic Explorer (nEASE). nEASE complements traditional gene ontology enrichment approaches by determining statistically enriched gene ontology subterms within a list of genes based on co-annotation. Here, we overview an open-source software version of the nEASE algorithm. nEASE can be used either stand-alone or as part of a pathway discovery pipeline. Availability: nEASE is implemented within the Multiple Experiment Viewer software package available at http://www.tm4.org/mev . Contact: cholmes@stats.ox.ac.uk Supplementary information: Supplementary data are available at Bioinformatics online.
    Print ISSN: 1367-4803
    Electronic ISSN: 1460-2059
    Topics: Biology , Computer Science , Medicine
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  • 2
    Publication Date: 2019
    Description: Accurately estimating aboveground biomass (AGB) is important in many applications, including monitoring carbon stocks, investigating deforestation and forest degradation, and designing sustainable forest management strategies. Although lidar provides critical three-dimensional forest structure information for estimating AGB, acquiring comprehensive lidar coverage is often cost prohibitive. This research focused on developing a lidar sampling framework to support AGB estimation from Landsat images. Two sampling strategies, systematic and classification-based, were tested and compared. The proposed strategies were implemented over a temperate forest study site in northern New York State and the processes were then validated at a similar site located in central New York State. Our results demonstrated that while the inclusion of lidar data using systematic or classification-based sampling supports AGB estimation, the systematic sampling selection method was highly dependent on site conditions and had higher accuracy variability. Of the 12 systematic sampling plans, R2 values ranged from 0.14 to 0.41 and plot root mean square error (RMSE) ranged from 84.2 to 93.9 Mg ha−1. The classification-based sampling outperformed 75% of the systematic sampling strategies at the primary site with R2 of 0.26 and RMSE of 70.1 Mg ha−1. The classification-based lidar sampling strategy was relatively easy to apply and was readily transferable to a new study site. Adopting this method at the validation site, the classification-based sampling also worked effectively, with an R2 of 0.40 and an RMSE of 108.2 Mg ha−1 compared to the full lidar coverage model with an R2 of 0.58 and an RMSE of 96.0 Mg ha−1. This study evaluated different lidar sample selection methods to identify an efficient and effective approach to reduce the volume and cost of lidar acquisitions. The forest type classification-based sampling method described in this study could facilitate cost-effective lidar data collection in future studies.
    Electronic ISSN: 2072-4292
    Topics: Architecture, Civil Engineering, Surveying , Geography
    Published by MDPI
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  • 3
    Publication Date: 2003-12-20
    Description: Approximately 80% of the maize genome comprises highly repetitive sequences interspersed with single-copy, gene-rich sequences, and standard genome sequencing strategies are not readily adaptable to this type of genome. Methodologies that enrich for genic sequences might more rapidly generate useful results from complex genomes. Equivalent numbers of clones from maize selected by techniques called methylation filtering and High C0t selection were sequenced to generate approximately 200,000 reads (approximately 132 megabases), which were assembled into contigs. Combination of the two techniques resulted in a sixfold reduction in the effective genome size and a fourfold increase in the gene identification rate in comparison to a nonenriched library.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Whitelaw, C A -- Barbazuk, W B -- Pertea, G -- Chan, A P -- Cheung, F -- Lee, Y -- Zheng, L -- van Heeringen, S -- Karamycheva, S -- Bennetzen, J L -- SanMiguel, P -- Lakey, N -- Bedell, J -- Yuan, Y -- Budiman, M A -- Resnick, A -- Van Aken, S -- Utterback, T -- Riedmuller, S -- Williams, M -- Feldblyum, T -- Schubert, K -- Beachy, R -- Fraser, C M -- Quackenbush, J -- New York, N.Y. -- Science. 2003 Dec 19;302(5653):2118-20.〈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/14684821" target="_blank"〉PubMed〈/a〉
    Keywords: Chromosomes, Plant/genetics ; Cloning, Molecular ; Computational Biology ; Contig Mapping ; DNA Methylation ; DNA, Plant/genetics ; Databases, Nucleic Acid ; Expressed Sequence Tags ; Gene Dosage ; Gene Library ; *Genes, Plant ; *Genome, Plant ; Molecular Sequence Data ; Repetitive Sequences, Nucleic Acid ; Retroelements ; Sequence Alignment ; Sequence Analysis, DNA/*methods ; Transcription, Genetic ; Zea mays/*genetics
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 4
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2003-10-11
    Description: DNA microarray analysis has provided a wealth of data on global patterns of gene expression but has yet to deliver on its early promise of identifying networks of interacting gene products. In his Perspective, Quackenbush discusses new work (Stuart et al.) that uses evolutionary conservation of gene expression patterns in yeast, worm, fruit fly, and human in an attempt to identify functionally related groups of genes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Quackenbush, John -- New York, N.Y. -- Science. 2003 Oct 10;302(5643):240-1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Institute for Genomic Research, 9712 Medical Center Drive, Rockville, MD 20850, USA. johnq@tigr.org〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14551426" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Caenorhabditis elegans/genetics ; Cell Cycle/genetics ; Cell Division/genetics ; Computational Biology ; Drosophila melanogaster/genetics ; *Gene Expression ; Gene Expression Profiling ; Gene Expression Regulation ; Genes, Fungal ; Genes, Helminth ; Genes, Insect ; Humans ; *Oligonucleotide Array Sequence Analysis ; RNA Splicing ; Saccharomyces cerevisiae/genetics ; Species Specificity
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 5
    Publication Date: 2005-09-06
    Description: This study describes comprehensive polling of transcription start and termination sites and analysis of previously unidentified full-length complementary DNAs derived from the mouse genome. We identify the 5' and 3' boundaries of 181,047 transcripts with extensive variation in transcripts arising from alternative promoter usage, splicing, and polyadenylation. There are 16,247 new mouse protein-coding transcripts, including 5154 encoding previously unidentified proteins. Genomic mapping of the transcriptome reveals transcriptional forests, with overlapping transcription on both strands, separated by deserts in which few transcripts are observed. The data provide a comprehensive platform for the comparative analysis of mammalian transcriptional regulation in differentiation and development.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Carninci, P -- Kasukawa, T -- Katayama, S -- Gough, J -- Frith, M C -- Maeda, N -- Oyama, R -- Ravasi, T -- Lenhard, B -- Wells, C -- Kodzius, R -- Shimokawa, K -- Bajic, V B -- Brenner, S E -- Batalov, S -- Forrest, A R R -- Zavolan, M -- Davis, M J -- Wilming, L G -- Aidinis, V -- Allen, J E -- Ambesi-Impiombato, A -- Apweiler, R -- Aturaliya, R N -- Bailey, T L -- Bansal, M -- Baxter, L -- Beisel, K W -- Bersano, T -- Bono, H -- Chalk, A M -- Chiu, K P -- Choudhary, V -- Christoffels, A -- Clutterbuck, D R -- Crowe, M L -- Dalla, E -- Dalrymple, B P -- de Bono, B -- Della Gatta, G -- di Bernardo, D -- Down, T -- Engstrom, P -- Fagiolini, M -- Faulkner, G -- Fletcher, C F -- Fukushima, T -- Furuno, M -- Futaki, S -- Gariboldi, M -- Georgii-Hemming, P -- Gingeras, T R -- Gojobori, T -- Green, R E -- Gustincich, S -- Harbers, M -- Hayashi, Y -- Hensch, T K -- Hirokawa, N -- Hill, D -- Huminiecki, L -- Iacono, M -- Ikeo, K -- Iwama, A -- Ishikawa, T -- Jakt, M -- Kanapin, A -- Katoh, M -- Kawasawa, Y -- Kelso, J -- Kitamura, H -- Kitano, H -- Kollias, G -- Krishnan, S P T -- Kruger, A -- Kummerfeld, S K -- Kurochkin, I V -- Lareau, L F -- Lazarevic, D -- Lipovich, L -- Liu, J -- Liuni, S -- McWilliam, S -- Madan Babu, M -- Madera, M -- Marchionni, L -- Matsuda, H -- Matsuzawa, S -- Miki, H -- Mignone, F -- Miyake, S -- Morris, K -- Mottagui-Tabar, S -- Mulder, N -- Nakano, N -- Nakauchi, H -- Ng, P -- Nilsson, R -- Nishiguchi, S -- Nishikawa, S -- Nori, F -- Ohara, O -- Okazaki, Y -- Orlando, V -- Pang, K C -- Pavan, W J -- Pavesi, G -- Pesole, G -- Petrovsky, N -- Piazza, S -- Reed, J -- Reid, J F -- Ring, B Z -- Ringwald, M -- Rost, B -- Ruan, Y -- Salzberg, S L -- Sandelin, A -- Schneider, C -- Schonbach, C -- Sekiguchi, K -- Semple, C A M -- Seno, S -- Sessa, L -- Sheng, Y -- Shibata, Y -- Shimada, H -- Shimada, K -- Silva, D -- Sinclair, B -- Sperling, S -- Stupka, E -- Sugiura, K -- Sultana, R -- Takenaka, Y -- Taki, K -- Tammoja, K -- Tan, S L -- Tang, S -- Taylor, M S -- Tegner, J -- Teichmann, S A -- Ueda, H R -- van Nimwegen, E -- Verardo, R -- Wei, C L -- Yagi, K -- Yamanishi, H -- Zabarovsky, E -- Zhu, S -- Zimmer, A -- Hide, W -- Bult, C -- Grimmond, S M -- Teasdale, R D -- Liu, E T -- Brusic, V -- Quackenbush, J -- Wahlestedt, C -- Mattick, J S -- Hume, D A -- Kai, C -- Sasaki, D -- Tomaru, Y -- Fukuda, S -- Kanamori-Katayama, M -- Suzuki, M -- Aoki, J -- Arakawa, T -- Iida, J -- Imamura, K -- Itoh, M -- Kato, T -- Kawaji, H -- Kawagashira, N -- Kawashima, T -- Kojima, M -- Kondo, S -- Konno, H -- Nakano, K -- Ninomiya, N -- Nishio, T -- Okada, M -- Plessy, C -- Shibata, K -- Shiraki, T -- Suzuki, S -- Tagami, M -- Waki, K -- Watahiki, A -- Okamura-Oho, Y -- Suzuki, H -- Kawai, J -- Hayashizaki, Y -- FANTOM Consortium -- RIKEN Genome Exploration Research Group and Genome Science Group (Genome Network Project Core Group) -- TGM03P17/Telethon/Italy -- TGM06S01/Telethon/Italy -- New York, N.Y. -- Science. 2005 Sep 2;309(5740):1559-63.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16141072" target="_blank"〉PubMed〈/a〉
    Keywords: 3' Untranslated Regions ; Animals ; Base Sequence ; Conserved Sequence ; DNA, Complementary/chemistry ; *Genome ; Genome, Human ; Genomics ; Humans ; Mice/*genetics ; Promoter Regions, Genetic ; Proteins/genetics ; RNA/chemistry/classification ; RNA Splicing ; RNA, Untranslated/chemistry ; Regulatory Sequences, Ribonucleic Acid ; *Terminator Regions, Genetic ; *Transcription Initiation Site ; *Transcription, Genetic
    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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  • 6
    Publication Date: 2002-10-22
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ball, Catherine A -- Sherlock, Gavin -- Parkinson, Helen -- Rocca-Sera, Philippe -- Brooksbank, Catherine -- Causton, Helen C -- Cavalieri, Duccio -- Gaasterland, Terry -- Hingamp, Pascal -- Holstege, Frank -- Ringwald, Martin -- Spellman, Paul -- Stoeckert, Christian J Jr -- Stewart, Jason E -- Taylor, Ronald -- Brazma, Alvis -- Quackenbush, John -- Microarray Gene Expression Data (MGED) Society -- New York, N.Y. -- Science. 2002 Oct 18;298(5593):539.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12387284" target="_blank"〉PubMed〈/a〉
    Keywords: *Computational Biology ; Databases, Nucleic Acid ; Gene Expression Profiling ; Guidelines as Topic ; Oligonucleotide Array Sequence Analysis/*standards ; Periodicals as Topic ; *Publishing ; Research Design/*standards
    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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  • 7
    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
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  • 8
    Publication Date: 2013-11-29
    Description: Two large-scale pharmacogenomic studies were published recently in this journal. Genomic data are well correlated between studies; however, the measured drug response data are highly discordant. Although the source of inconsistencies remains uncertain, it has potential implications for using these outcome measures to assess gene-drug associations or select potential anticancer drugs on the basis of their reported results.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4237165/" 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/PMC4237165/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Haibe-Kains, Benjamin -- El-Hachem, Nehme -- Birkbak, Nicolai Juul -- Jin, Andrew C -- Beck, Andrew H -- Aerts, Hugo J W L -- Quackenbush, John -- CA087969/CA/NCI NIH HHS/ -- P01 CA087969/CA/NCI NIH HHS/ -- U19 CA148065/CA/NCI NIH HHS/ -- U19 CA148065-01/CA/NCI NIH HHS/ -- England -- Nature. 2013 Dec 19;504(7480):389-93. doi: 10.1038/nature12831. Epub 2013 Nov 27.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Institut de Recherches Cliniques de Montreal, University of Montreal, Montreal, Quebec, Canada [2] Ontario Cancer Institute, Princess Margaret Cancer Centre, University Health Network, Toronto, Ontario M5G 2M9, Canada. ; Institut de Recherches Cliniques de Montreal, University of Montreal, Montreal, Quebec, Canada. ; Center for Biological Sequence Analysis, Department of Systems Biology, Technical University of Denmark, 2800 Kgs, Lyngby, Denmark. ; Department of Pathology, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts 02215, USA. ; 1] Department of Pathology, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts 02215, USA [2]. ; 1] Department of Biostatistics and Computational Biology and Center for Cancer Computational Biology, Dana-Farber Cancer Institute, Boston, Massachusetts 02215, USA [2] Department of Radiation Oncology & Radiology, Dana-Farber Cancer Institute, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts 02215, USA [3] Department of Radiation Oncology, Maastricht University, Maastricht 6200 MD, The Netherlands [4]. ; 1] Department of Biostatistics and Computational Biology and Center for Cancer Computational Biology, Dana-Farber Cancer Institute, Boston, Massachusetts 02215, USA [2] Department of Cancer Biology, Dana-Farber Cancer Institute, Boston, Massachusetts 02215, USA [3].〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24284626" target="_blank"〉PubMed〈/a〉
    Keywords: Antineoplastic Agents/*pharmacology ; Area Under Curve ; Cell Line ; Drug Resistance, Neoplasm/drug effects/genetics ; Gene Expression Profiling ; Genome, Human/genetics ; Humans ; Inhibitory Concentration 50 ; Neoplasms/drug therapy/genetics/pathology ; *Pharmacogenetics ; Reproducibility of Results
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  • 9
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    Unknown
    Nature Publishing Group (NPG)
    Publication Date: 2014-05-30
    Description: 〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4205237/" 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/PMC4205237/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Quackenbush, John -- R01 HL111759/HL/NHLBI NIH HHS/ -- England -- Nature. 2014 May 29;509(7502):S68. doi: 10.1038/509S68a.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Cancer Computational Biology at the Dana-Farber Cancer Institute in Boston, Massachusetts.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24870827" target="_blank"〉PubMed〈/a〉
    Keywords: Biomedical Research/methods ; Human Genome Project ; Humans ; *Information Dissemination/methods ; *Knowledge Bases ; Neoplasms/*genetics/therapy
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 10
    Publication Date: 2011-06-10
    Description: Cyclin D1 is a component of the core cell cycle machinery. Abnormally high levels of cyclin D1 are detected in many human cancer types. To elucidate the molecular functions of cyclin D1 in human cancers, we performed a proteomic screen for cyclin D1 protein partners in several types of human tumours. Analyses of cyclin D1 interactors revealed a network of DNA repair proteins, including RAD51, a recombinase that drives the homologous recombination process. We found that cyclin D1 directly binds RAD51, and that cyclin D1-RAD51 interaction is induced by radiation. Like RAD51, cyclin D1 is recruited to DNA damage sites in a BRCA2-dependent fashion. Reduction of cyclin D1 levels in human cancer cells impaired recruitment of RAD51 to damaged DNA, impeded the homologous recombination-mediated DNA repair, and increased sensitivity of cells to radiation in vitro and in vivo. This effect was seen in cancer cells lacking the retinoblastoma protein, which do not require D-cyclins for proliferation. These findings reveal an unexpected function of a core cell cycle protein in DNA repair and suggest that targeting cyclin D1 may be beneficial also in retinoblastoma-negative cancers which are currently thought to be unaffected by cyclin D1 inhibition.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3134411/" 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/PMC3134411/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jirawatnotai, Siwanon -- Hu, Yiduo -- Michowski, Wojciech -- Elias, Joshua E -- Becks, Lisa -- Bienvenu, Frederic -- Zagozdzon, Agnieszka -- Goswami, Tapasree -- Wang, Yaoyu E -- Clark, Alan B -- Kunkel, Thomas A -- van Harn, Tanja -- Xia, Bing -- Correll, Mick -- Quackenbush, John -- Livingston, David M -- Gygi, Steven P -- Sicinski, Piotr -- P01 CA080111/CA/NCI NIH HHS/ -- P01 CA080111-12/CA/NCI NIH HHS/ -- P01 CA109901/CA/NCI NIH HHS/ -- P01 CA109901-07/CA/NCI NIH HHS/ -- P30 AI060354/AI/NIAID NIH HHS/ -- R01 CA083688/CA/NCI NIH HHS/ -- R01 CA083688-10/CA/NCI NIH HHS/ -- R01 CA138804/CA/NCI NIH HHS/ -- R01 CA138804-02/CA/NCI NIH HHS/ -- Z01 ES065089-11/Intramural NIH HHS/ -- England -- Nature. 2011 Jun 8;474(7350):230-4. doi: 10.1038/nature10155.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cancer Biology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts 02215, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21654808" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line, Tumor ; Comet Assay ; Cyclin D1/deficiency/*metabolism ; DNA Damage/radiation effects ; *DNA Repair/radiation effects ; HeLa Cells ; Humans ; Mice ; Neoplasms/genetics/*metabolism/pathology ; Protein Binding/radiation effects ; *Protein Interaction Mapping ; Rad51 Recombinase/*metabolism ; Radiation, Ionizing ; Recombination, Genetic/genetics ; Retinoblastoma Protein/deficiency
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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