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  • 1
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    Genome-scale DNA methylation maps of pluripotent and differentiated cells (2008)
    Nature Publishing Group (NPG)
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    Publication Date: 2008-07-05
    Description: DNA methylation is essential for normal development and has been implicated in many pathologies including cancer. Our knowledge about the genome-wide distribution of DNA methylation, how it changes during cellular differentiation and how it relates to histone methylation and other chromatin modifications in mammals remains limited. Here we report the generation and analysis of genome-scale DNA methylation profiles at nucleotide resolution in mammalian cells. Using high-throughput reduced representation bisulphite sequencing and single-molecule-based sequencing, we generated DNA methylation maps covering most CpG islands, and a representative sampling of conserved non-coding elements, transposons and other genomic features, for mouse embryonic stem cells, embryonic-stem-cell-derived and primary neural cells, and eight other primary tissues. Several key findings emerge from the data. First, DNA methylation patterns are better correlated with histone methylation patterns than with the underlying genome sequence context. Second, methylation of CpGs are dynamic epigenetic marks that undergo extensive changes during cellular differentiation, particularly in regulatory regions outside of core promoters. Third, analysis of embryonic-stem-cell-derived and primary cells reveals that 'weak' CpG islands associated with a specific set of developmentally regulated genes undergo aberrant hypermethylation during extended proliferation in vitro, in a pattern reminiscent of that reported in some primary tumours. More generally, the results establish reduced representation bisulphite sequencing as a powerful technology for epigenetic profiling of cell populations relevant to developmental biology, cancer and regenerative medicine.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2896277/" 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/PMC2896277/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Meissner, Alexander -- Mikkelsen, Tarjei S -- Gu, Hongcang -- Wernig, Marius -- Hanna, Jacob -- Sivachenko, Andrey -- Zhang, Xiaolan -- Bernstein, Bradley E -- Nusbaum, Chad -- Jaffe, David B -- Gnirke, Andreas -- Jaenisch, Rudolf -- Lander, Eric S -- R01 HG004401/HG/NHGRI NIH HHS/ -- R01 HG004401-02/HG/NHGRI NIH HHS/ -- U54 HG003067/HG/NHGRI NIH HHS/ -- U54 HG003067-04/HG/NHGRI NIH HHS/ -- U54 HG003067-06/HG/NHGRI NIH HHS/ -- England -- Nature. 2008 Aug 7;454(7205):766-70. doi: 10.1038/nature07107. Epub 2008 Jul 6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Whitehead Institute for Biomedical Research, 9 Cambridge Center, Cambridge, Massachusetts 02142, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18600261" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Cell Differentiation ; Cells, Cultured ; Conserved Sequence ; CpG Islands/genetics ; *DNA Methylation ; Embryonic Stem Cells/cytology/metabolism ; Fibroblasts/cytology ; Genome/genetics ; *Genomics ; Histones/genetics/metabolism ; Male ; Mice ; Neurons/cytology ; Pluripotent Stem Cells/*cytology/*metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 2
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    Dissecting direct reprogramming through integrative genomic analysis (2008)
    Nature Publishing Group (NPG)
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    Publication Date: 2008-05-30
    Description: Somatic cells can be reprogrammed to a pluripotent state through the ectopic expression of defined transcription factors. Understanding the mechanism and kinetics of this transformation may shed light on the nature of developmental potency and suggest strategies with improved efficiency or safety. Here we report an integrative genomic analysis of reprogramming of mouse fibroblasts and B lymphocytes. Lineage-committed cells show a complex response to the ectopic expression involving induction of genes downstream of individual reprogramming factors. Fully reprogrammed cells show gene expression and epigenetic states that are highly similar to embryonic stem cells. In contrast, stable partially reprogrammed cell lines show reactivation of a distinctive subset of stem-cell-related genes, incomplete repression of lineage-specifying transcription factors, and DNA hypermethylation at pluripotency-related loci. These observations suggest that some cells may become trapped in partially reprogrammed states owing to incomplete repression of transcription factors, and that DNA de-methylation is an inefficient step in the transition to pluripotency. We demonstrate that RNA inhibition of transcription factors can facilitate reprogramming, and that treatment with DNA methyltransferase inhibitors can improve the overall efficiency of the reprogramming process.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2754827/" 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/PMC2754827/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mikkelsen, Tarjei S -- Hanna, Jacob -- Zhang, Xiaolan -- Ku, Manching -- Wernig, Marius -- Schorderet, Patrick -- Bernstein, Bradley E -- Jaenisch, Rudolf -- Lander, Eric S -- Meissner, Alexander -- U54 HG003067/HG/NHGRI NIH HHS/ -- U54 HG003067-04/HG/NHGRI NIH HHS/ -- England -- Nature. 2008 Jul 3;454(7200):49-55. doi: 10.1038/nature07056. Epub 2008 May 28.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Broad Institute of MIT and Harvard, 7 Cambridge Center, Cambridge, Massachusetts 02142, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18509334" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Azacitidine/pharmacology ; Cell Line ; Cell Lineage ; Cellular Reprogramming/*genetics ; Chromatin/metabolism ; DNA (Cytosine-5-)-Methyltransferase/antagonists & inhibitors/genetics/metabolism ; DNA Methylation ; Embryonic Stem Cells/metabolism ; Enzyme Inhibitors/pharmacology ; Gene Expression Profiling ; Gene Expression Regulation, Developmental ; Genome/genetics ; *Genomics ; Mice ; Pluripotent Stem Cells/cytology/*metabolism ; Transcription Factors/deficiency/genetics
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 3
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    Sequencing the nuclear genome of the extinct woolly mammoth (2008)
    Nature Publishing Group (NPG)
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    Publication Date: 2008-11-21
    Description: In 1994, two independent groups extracted DNA from several Pleistocene epoch mammoths and noted differences among individual specimens. Subsequently, DNA sequences have been published for a number of extinct species. However, such ancient DNA is often fragmented and damaged, and studies to date have typically focused on short mitochondrial sequences, never yielding more than a fraction of a per cent of any nuclear genome. Here we describe 4.17 billion bases (Gb) of sequence from several mammoth specimens, 3.3 billion (80%) of which are from the woolly mammoth (Mammuthus primigenius) genome and thus comprise an extensive set of genome-wide sequence from an extinct species. Our data support earlier reports that elephantid genomes exceed 4 Gb. The estimated divergence rate between mammoth and African elephant is half of that between human and chimpanzee. The observed number of nucleotide differences between two particular mammoths was approximately one-eighth of that between one of them and the African elephant, corresponding to a separation between the mammoths of 1.5-2.0 Myr. The estimated probability that orthologous elephant and mammoth amino acids differ is 0.002, corresponding to about one residue per protein. Differences were discovered between mammoth and African elephant in amino-acid positions that are otherwise invariant over several billion years of combined mammalian evolution. This study shows that nuclear genome sequencing of extinct species can reveal population differences not evident from the fossil record, and perhaps even discover genetic factors that affect extinction.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Miller, Webb -- Drautz, Daniela I -- Ratan, Aakrosh -- Pusey, Barbara -- Qi, Ji -- Lesk, Arthur M -- Tomsho, Lynn P -- Packard, Michael D -- Zhao, Fangqing -- Sher, Andrei -- Tikhonov, Alexei -- Raney, Brian -- Patterson, Nick -- Lindblad-Toh, Kerstin -- Lander, Eric S -- Knight, James R -- Irzyk, Gerard P -- Fredrikson, Karin M -- Harkins, Timothy T -- Sheridan, Sharon -- Pringle, Tom -- Schuster, Stephan C -- HG002238/HG/NHGRI NIH HHS/ -- England -- Nature. 2008 Nov 20;456(7220):387-90. doi: 10.1038/nature07446.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Pennsylvania State University, Center for Comparative Genomics and Bioinformatics, 310 Wartik Building, University Park, Pennsylvania 16802, USA. webb@bx.psu.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19020620" target="_blank"〉PubMed〈/a〉
    Keywords: Africa ; Animals ; Cell Nucleus/*genetics ; Conserved Sequence/genetics ; Elephants/anatomy & histology/*genetics ; *Evolution, Molecular ; *Extinction, Biological ; Female ; *Fossils ; Genome/*genetics ; *Genomics ; Hair/metabolism ; Humans ; India ; Male ; Phylogeny ; Sequence Analysis, DNA/*methods
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 4
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    Somatic mutations affect key pathways in lung adenocarcinoma (2008)
    Nature Publishing Group (NPG)
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    Publication Date: 2008-10-25
    Description: Determining the genetic basis of cancer requires comprehensive analyses of large collections of histopathologically well-classified primary tumours. Here we report the results of a collaborative study to discover somatic mutations in 188 human lung adenocarcinomas. DNA sequencing of 623 genes with known or potential relationships to cancer revealed more than 1,000 somatic mutations across the samples. Our analysis identified 26 genes that are mutated at significantly high frequencies and thus are probably involved in carcinogenesis. The frequently mutated genes include tyrosine kinases, among them the EGFR homologue ERBB4; multiple ephrin receptor genes, notably EPHA3; vascular endothelial growth factor receptor KDR; and NTRK genes. These data provide evidence of somatic mutations in primary lung adenocarcinoma for several tumour suppressor genes involved in other cancers--including NF1, APC, RB1 and ATM--and for sequence changes in PTPRD as well as the frequently deleted gene LRP1B. The observed mutational profiles correlate with clinical features, smoking status and DNA repair defects. These results are reinforced by data integration including single nucleotide polymorphism array and gene expression array. Our findings shed further light on several important signalling pathways involved in lung adenocarcinoma, and suggest new molecular targets for treatment.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2694412/" 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/PMC2694412/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ding, Li -- Getz, Gad -- Wheeler, David A -- Mardis, Elaine R -- McLellan, Michael D -- Cibulskis, Kristian -- Sougnez, Carrie -- Greulich, Heidi -- Muzny, Donna M -- Morgan, Margaret B -- Fulton, Lucinda -- Fulton, Robert S -- Zhang, Qunyuan -- Wendl, Michael C -- Lawrence, Michael S -- Larson, David E -- Chen, Ken -- Dooling, David J -- Sabo, Aniko -- Hawes, Alicia C -- Shen, Hua -- Jhangiani, Shalini N -- Lewis, Lora R -- Hall, Otis -- Zhu, Yiming -- Mathew, Tittu -- Ren, Yanru -- Yao, Jiqiang -- Scherer, Steven E -- Clerc, Kerstin -- Metcalf, Ginger A -- Ng, Brian -- Milosavljevic, Aleksandar -- Gonzalez-Garay, Manuel L -- Osborne, John R -- Meyer, Rick -- Shi, Xiaoqi -- Tang, Yuzhu -- Koboldt, Daniel C -- Lin, Ling -- Abbott, Rachel -- Miner, Tracie L -- Pohl, Craig -- Fewell, Ginger -- Haipek, Carrie -- Schmidt, Heather -- Dunford-Shore, Brian H -- Kraja, Aldi -- Crosby, Seth D -- Sawyer, Christopher S -- Vickery, Tammi -- Sander, Sacha -- Robinson, Jody -- Winckler, Wendy -- Baldwin, Jennifer -- Chirieac, Lucian R -- Dutt, Amit -- Fennell, Tim -- Hanna, Megan -- Johnson, Bruce E -- Onofrio, Robert C -- Thomas, Roman K -- Tonon, Giovanni -- Weir, Barbara A -- Zhao, Xiaojun -- Ziaugra, Liuda -- Zody, Michael C -- Giordano, Thomas -- Orringer, Mark B -- Roth, Jack A -- Spitz, Margaret R -- Wistuba, Ignacio I -- Ozenberger, Bradley -- Good, Peter J -- Chang, Andrew C -- Beer, David G -- Watson, Mark A -- Ladanyi, Marc -- Broderick, Stephen -- Yoshizawa, Akihiko -- Travis, William D -- Pao, William -- Province, Michael A -- Weinstock, George M -- Varmus, Harold E -- Gabriel, Stacey B -- Lander, Eric S -- Gibbs, Richard A -- Meyerson, Matthew -- Wilson, Richard K -- P50 CA070907/CA/NCI NIH HHS/ -- R01 CA154365/CA/NCI NIH HHS/ -- U19 CA084953/CA/NCI NIH HHS/ -- U19 CA084953-050003/CA/NCI NIH HHS/ -- U54 HG003067/HG/NHGRI NIH HHS/ -- U54 HG003067-04/HG/NHGRI NIH HHS/ -- U54 HG003273/HG/NHGRI NIH HHS/ -- England -- Nature. 2008 Oct 23;455(7216):1069-75. doi: 10.1038/nature07423.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Genome Center at Washington University, Department of Genetics, Washington University School of Medicine, St Louis, Missouri 63108, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18948947" target="_blank"〉PubMed〈/a〉
    Keywords: Adenocarcinoma, Bronchiolo-Alveolar/*genetics ; Female ; Gene Dosage ; Gene Expression Regulation, Neoplastic ; Genes, Tumor Suppressor ; Humans ; Lung Neoplasms/*genetics ; Male ; Mutation/*genetics ; Proto-Oncogenes/genetics
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 5
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    Chromatin signature reveals over a thousand highly conserved large non-coding RNAs in mammals (2009)
    Nature Publishing Group (NPG)
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    Publication Date: 2009-02-03
    Description: There is growing recognition that mammalian cells produce many thousands of large intergenic transcripts. However, the functional significance of these transcripts has been particularly controversial. Although there are some well-characterized examples, most (〉95%) show little evidence of evolutionary conservation and have been suggested to represent transcriptional noise. Here we report a new approach to identifying large non-coding RNAs using chromatin-state maps to discover discrete transcriptional units intervening known protein-coding loci. Our approach identified approximately 1,600 large multi-exonic RNAs across four mouse cell types. In sharp contrast to previous collections, these large intervening non-coding RNAs (lincRNAs) show strong purifying selection in their genomic loci, exonic sequences and promoter regions, with greater than 95% showing clear evolutionary conservation. We also developed a functional genomics approach that assigns putative functions to each lincRNA, demonstrating a diverse range of roles for lincRNAs in processes from embryonic stem cell pluripotency to cell proliferation. We obtained independent functional validation for the predictions for over 100 lincRNAs, using cell-based assays. In particular, we demonstrate that specific lincRNAs are transcriptionally regulated by key transcription factors in these processes such as p53, NFkappaB, Sox2, Oct4 (also known as Pou5f1) and Nanog. Together, these results define a unique collection of functional lincRNAs that are highly conserved and implicated in diverse biological processes.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2754849/" 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/PMC2754849/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Guttman, Mitchell -- Amit, Ido -- Garber, Manuel -- French, Courtney -- Lin, Michael F -- Feldser, David -- Huarte, Maite -- Zuk, Or -- Carey, Bryce W -- Cassady, John P -- Cabili, Moran N -- Jaenisch, Rudolf -- Mikkelsen, Tarjei S -- Jacks, Tyler -- Hacohen, Nir -- Bernstein, Bradley E -- Kellis, Manolis -- Regev, Aviv -- Rinn, John L -- Lander, Eric S -- DP1 OD003958/OD/NIH HHS/ -- R01 HG004037/HG/NHGRI NIH HHS/ -- R01 HG004037-02/HG/NHGRI NIH HHS/ -- U54 HG003067/HG/NHGRI NIH HHS/ -- U54 HG003067-05/HG/NHGRI NIH HHS/ -- England -- Nature. 2009 Mar 12;458(7235):223-7. doi: 10.1038/nature07672. Epub 2009 Feb 1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Broad Institute of MIT and Harvard, 7 Cambridge Center, Cambridge, Massachusetts 02142, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19182780" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Cells, Cultured ; Chromatin/*genetics ; *Conserved Sequence/genetics ; DNA, Intergenic ; Exons/genetics ; Mammals/*genetics ; Mice ; Promoter Regions, Genetic/genetics ; RNA/*genetics ; Reproducibility of Results ; Transcription Factors/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
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    Systematic RNA interference reveals that oncogenic KRAS-driven cancers require TBK1 (2009)
    Nature Publishing Group (NPG)
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    Publication Date: 2009-10-23
    Description: The proto-oncogene KRAS is mutated in a wide array of human cancers, most of which are aggressive and respond poorly to standard therapies. Although the identification of specific oncogenes has led to the development of clinically effective, molecularly targeted therapies in some cases, KRAS has remained refractory to this approach. A complementary strategy for targeting KRAS is to identify gene products that, when inhibited, result in cell death only in the presence of an oncogenic allele. Here we have used systematic RNA interference to detect synthetic lethal partners of oncogenic KRAS and found that the non-canonical IkappaB kinase TBK1 was selectively essential in cells that contain mutant KRAS. Suppression of TBK1 induced apoptosis specifically in human cancer cell lines that depend on oncogenic KRAS expression. In these cells, TBK1 activated NF-kappaB anti-apoptotic signals involving c-Rel and BCL-XL (also known as BCL2L1) that were essential for survival, providing mechanistic insights into this synthetic lethal interaction. These observations indicate that TBK1 and NF-kappaB signalling are essential in KRAS mutant tumours, and establish a general approach for the rational identification of co-dependent pathways in cancer.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2783335/" 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/PMC2783335/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barbie, David A -- Tamayo, Pablo -- Boehm, Jesse S -- Kim, So Young -- Moody, Susan E -- Dunn, Ian F -- Schinzel, Anna C -- Sandy, Peter -- Meylan, Etienne -- Scholl, Claudia -- Frohling, Stefan -- Chan, Edmond M -- Sos, Martin L -- Michel, Kathrin -- Mermel, Craig -- Silver, Serena J -- Weir, Barbara A -- Reiling, Jan H -- Sheng, Qing -- Gupta, Piyush B -- Wadlow, Raymond C -- Le, Hanh -- Hoersch, Sebastian -- Wittner, Ben S -- Ramaswamy, Sridhar -- Livingston, David M -- Sabatini, David M -- Meyerson, Matthew -- Thomas, Roman K -- Lander, Eric S -- Mesirov, Jill P -- Root, David E -- Gilliland, D Gary -- Jacks, Tyler -- Hahn, William C -- R01 CA129105/CA/NCI NIH HHS/ -- R01 CA129105-03/CA/NCI NIH HHS/ -- R01 CA130988/CA/NCI NIH HHS/ -- R01 CA130988-01A2/CA/NCI NIH HHS/ -- R33 CA128625/CA/NCI NIH HHS/ -- R33 CA128625-01A1/CA/NCI NIH HHS/ -- R33 CA128625-02/CA/NCI NIH HHS/ -- T32 CA009172/CA/NCI NIH HHS/ -- T32 CA09172-33/CA/NCI NIH HHS/ -- T32 GM007753/GM/NIGMS NIH HHS/ -- England -- Nature. 2009 Nov 5;462(7269):108-12. doi: 10.1038/nature08460. Epub 2009 Oct 21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medical Oncology, Dana-Farber Cancer Institute, 44 Binney Street, Boston, Massachusetts 02115 USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19847166" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Apoptosis ; Cell Line, Tumor ; Cell Survival ; Gene Expression Profiling ; Genes, Lethal ; Genes, ras/*genetics ; Humans ; Lung Neoplasms/genetics/metabolism/pathology ; Neoplasms/genetics/metabolism/pathology ; Oncogene Protein p21(ras)/*genetics/*metabolism ; Protein-Serine-Threonine Kinases/antagonists & inhibitors/*metabolism ; Proto-Oncogene Proteins c-rel/metabolism ; *RNA Interference ; Signal Transduction ; bcl-X Protein/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 7
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    Comment on "The consensus coding sequences of human breast and colorectal cancers" (2007)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2007-09-18
    Description: Sjoblom et al. (Research Article, 13 October 2006, p. 268) reported nearly 200 novel cancer genes said to have a 90% probability of being involved in colon or breast cancer. However, their analysis raises two statistical concerns. When these concerns are addressed, few genes with significantly elevated mutation rates remain. Although the biological methodology in Sjoblom et al. is sound, more samples are needed to achieve sufficient power.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Getz, Gad -- Hofling, Holger -- Mesirov, Jill P -- Golub, Todd R -- Meyerson, Matthew -- Tibshirani, Robert -- Lander, Eric S -- New York, N.Y. -- Science. 2007 Sep 14;317(5844):1500.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Broad Institute of Massachusetts Institute of Technology and Harvard University, Cambridge, MA 02142, USA. gadgetz@broad.mit.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17872428" target="_blank"〉PubMed〈/a〉
    Keywords: Breast Neoplasms/*genetics ; Colorectal Neoplasms/*genetics ; *Consensus Sequence ; Female ; *Genes, Neoplasm ; Genome, Human ; Humans ; Male ; *Mutation ; Probability
    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
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    Genetic mapping in human disease (2008)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2008-11-08
    Description: Genetic mapping provides a powerful approach to identify genes and biological processes underlying any trait influenced by inheritance, including human diseases. We discuss the intellectual foundations of genetic mapping of Mendelian and complex traits in humans, examine lessons emerging from linkage analysis of Mendelian diseases and genome-wide association studies of common diseases, and discuss questions and challenges that lie ahead.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2694957/" 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/PMC2694957/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Altshuler, David -- Daly, Mark J -- Lander, Eric S -- U54 HG003067/HG/NHGRI NIH HHS/ -- U54 HG003067-03/HG/NHGRI NIH HHS/ -- New York, N.Y. -- Science. 2008 Nov 7;322(5903):881-8. doi: 10.1126/science.1156409.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Broad Institute of Harvard and MIT, Cambridge, MA 02142, USA. altshuler@molbio.mgh.harvard.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18988837" target="_blank"〉PubMed〈/a〉
    Keywords: *Chromosome Mapping ; Cloning, Molecular ; Disease/*genetics ; Genetic Linkage ; *Genome, Human ; *Genome-Wide Association Study ; Genotype ; Humans ; Linkage Disequilibrium ; Mutation ; Physical Chromosome Mapping ; Polymorphism, Single Nucleotide ; Quantitative Trait, Heritable ; Risk Factors ; Selection, 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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  • 9
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    The Connectivity Map: using gene-expression signatures to connect small molecules, genes, and disease (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-09-30
    Description: To pursue a systematic approach to the discovery of functional connections among diseases, genetic perturbation, and drug action, we have created the first installment of a reference collection of gene-expression profiles from cultured human cells treated with bioactive small molecules, together with pattern-matching software to mine these data. We demonstrate that this "Connectivity Map" resource can be used to find connections among small molecules sharing a mechanism of action, chemicals and physiological processes, and diseases and drugs. These results indicate the feasibility of the approach and suggest the value of a large-scale community Connectivity Map project.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lamb, Justin -- Crawford, Emily D -- Peck, David -- Modell, Joshua W -- Blat, Irene C -- Wrobel, Matthew J -- Lerner, Jim -- Brunet, Jean-Philippe -- Subramanian, Aravind -- Ross, Kenneth N -- Reich, Michael -- Hieronymus, Haley -- Wei, Guo -- Armstrong, Scott A -- Haggarty, Stephen J -- Clemons, Paul A -- Wei, Ru -- Carr, Steven A -- Lander, Eric S -- Golub, Todd R -- New York, N.Y. -- Science. 2006 Sep 29;313(5795):1929-35.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Broad Institute of Massachusetts Institute of Technology and Harvard University, Cambridge, MA 02142, USA. justin@broad.mit.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17008526" target="_blank"〉PubMed〈/a〉
    Keywords: Alzheimer Disease/drug therapy/genetics ; Cell Line ; Cell Line, Tumor ; *Databases, Factual ; Dexamethasone/pharmacology/therapeutic use ; Drug Evaluation, Preclinical/*methods ; Drug Resistance, Neoplasm ; Enzyme Inhibitors/pharmacology ; Estrogens/pharmacology ; Gene Expression/*drug effects ; *Gene Expression Profiling ; HSP90 Heat-Shock Proteins/antagonists & inhibitors ; Histone Deacetylase Inhibitors ; Humans ; Limonins/pharmacology ; Obesity/genetics/physiopathology ; Oligonucleotide Array Sequence Analysis ; Phenothiazines/pharmacology ; Precursor Cell Lymphoblastic Leukemia-Lymphoma/drug ; therapy/genetics/physiopathology ; Sirolimus/pharmacology/therapeutic use ; Software
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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    Positive natural selection in the human lineage (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-06-17
    Description: Positive natural selection is the force that drives the increase in prevalence of advantageous traits, and it has played a central role in our development as a species. Until recently, the study of natural selection in humans has largely been restricted to comparing individual candidate genes to theoretical expectations. The advent of genome-wide sequence and polymorphism data brings fundamental new tools to the study of natural selection. It is now possible to identify new candidates for selection and to reevaluate previous claims by comparison with empirical distributions of DNA sequence variation across the human genome and among populations. The flood of data and analytical methods, however, raises many new challenges. Here, we review approaches to detect positive natural selection, describe results from recent analyses of genome-wide data, and discuss the prospects and challenges ahead as we expand our understanding of the role of natural selection in shaping the human genome.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sabeti, P C -- Schaffner, S F -- Fry, B -- Lohmueller, J -- Varilly, P -- Shamovsky, O -- Palma, A -- Mikkelsen, T S -- Altshuler, D -- Lander, E S -- New York, N.Y. -- Science. 2006 Jun 16;312(5780):1614-20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Broad Institute of MIT and Harvard, Cambridge, MA, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16778047" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Biological Evolution ; Gene Frequency ; Genetic Variation ; Genetics, Population ; *Genome, Human ; Haplotypes ; Humans ; Mutation ; Polymorphism, Genetic ; *Selection, Genetic ; Sequence Analysis, DNA
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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