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  • 1
    Publication Date: 2015-10-07
    Description: The use of restricted maximum likelihood (REML) to estimate the heritability explained by common SNPs in a genome-wide association study (GWAS) of quantitative traits was proposed by Yang et al. (1) and implemented in the widely used GCTA software. Lee et al. (reference 2 in ref. 2) tries to extend...
    Keywords: Letters
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
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  • 2
    Publication Date: 2015-12-09
    Description: Article The oncogenic events driving indolent chronic lymphocytic leukaemia are relatively unknown. Here, the authors perform whole genome sequencing on 30 such tumours and identify recurrent mutations in IGLL5 and two activation induced cytidine deaminase signatures that are operative at different stages of CLL evolution. Nature Communications doi: 10.1038/ncomms9866 Authors: S. Kasar, J. Kim, R. Improgo, G. Tiao, P. Polak, N. Haradhvala, M. S. Lawrence, A. Kiezun, S. M. Fernandes, S. Bahl, C. Sougnez, S. Gabriel, E. S. Lander, H. T. Kim, G. Getz, J. R. Brown
    Electronic ISSN: 2041-1723
    Topics: Biology , Chemistry and Pharmacology , Natural Sciences in General , Physics
    Published by Springer Nature
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  • 3
    Publication Date: 2012-03-07
    Description: To gain insight into the genomic basis of diffuse large B-cell lymphoma (DLBCL), we performed massively parallel whole-exome sequencing of 55 primary tumor samples from patients with DLBCL and matched normal tissue. We identified recurrent mutations in genes that are well known to be functionally relevant in DLBCL, including MYD88, CARD11, EZH2, and CREBBP. We also identified somatic mutations in genes for which a functional role in DLBCL has not been previously suspected. These genes include MEF2B, MLL2, BTG1, GNA13, ACTB, P2RY8, PCLO, and TNFRSF14. Further, we show that BCL2 mutations commonly occur in patients with BCL2/IgH rearrangements as a result of somatic hypermutation normally occurring at the IgH locus. The BCL2 point mutations are primarily synonymous, and likely caused by activation-induced cytidine deaminase–mediated somatic hypermutation, as shown by comprehensive analysis of enrichment of mutations in WRCY target motifs. Those nonsynonymous mutations that are observed tend to be found outside of the functionally important BH domains of the protein, suggesting that strong negative selection against BCL2 loss-of-function mutations is at play. Last, by using an algorithm designed to identify likely functionally relevant but infrequent mutations, we identify KRAS, BRAF, and NOTCH1 as likely drivers of DLBCL pathogenesis in some patients. Our data provide an unbiased view of the landscape of mutations in DLBCL, and this in turn may point toward new therapeutic strategies for the disease.
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
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  • 4
    Publication Date: 1999-01-23
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pardes, H -- Manton, K G -- Lander, E S -- Tolley, H D -- Ullian, A D -- Palmer, H -- New York, N.Y. -- Science. 1999 Jan 1;283(5398):36-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Faculty of Medicine, College of Physicians and Surgeons, Columbia University, New York, NY 10032, USA. hp2@columbia.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9917262" target="_blank"〉PubMed〈/a〉
    Keywords: Aged ; *Biotechnology/economics ; *Delivery of Health Care ; Disabled Persons ; Drug Industry ; *Economics, Medical ; *Health Care Costs ; Health Status ; Humans ; Longevity ; *Research ; United States
    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
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1999-07-10
    Description: Microarray-based gene expression analysis identified genes showing ploidy-dependent expression in isogenic Saccharomyces cerevisiae strains that varied in ploidy from haploid to tetraploid. These genes were induced or repressed in proportion to the number of chromosome sets, regardless of the mating type. Ploidy-dependent repression of some G1 cyclins can explain the greater cell size associated with higher ploidies, and suggests ploidy-dependent modifications of cell cycle progression. Moreover, ploidy regulation of the FLO11 gene had direct consequences for yeast development.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Galitski, T -- Saldanha, A J -- Styles, C A -- Lander, E S -- Fink, G R -- GM35010/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1999 Jul 9;285(5425):251-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Whitehead Institute for Biomedical Research, 9 Cambridge Center, Cambridge, MA 02142, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10398601" target="_blank"〉PubMed〈/a〉
    Keywords: Chitinase/genetics ; Cyclins/genetics ; Fungal Proteins/genetics ; G1 Phase ; *Gene Expression Regulation, Fungal ; Haploidy ; Lipoproteins/genetics/physiology ; Membrane Glycoproteins ; Membrane Proteins/genetics ; Oligonucleotide Array Sequence Analysis ; Peptides/genetics/physiology ; Pheromones ; *Ploidies ; Polyploidy ; Saccharomyces cerevisiae/cytology/*genetics/physiology ; *Saccharomyces cerevisiae Proteins ; Transcription Factors/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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  • 6
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2001-02-07
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lander, E S -- Weinberg, R A -- New York, N.Y. -- Science. 2000 Mar 10;287(5459):1777-82.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology at the Massachusetts Institute of Technology, Cambridge, MA 02142, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10755930" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chromosome Mapping ; Chromosomes/genetics ; Cloning, Molecular ; DNA/chemistry/genetics ; DNA, Recombinant ; Evolution, Molecular ; Genes ; Genetic Code ; Genetics/*history/trends ; Genetics, Medical/history/trends ; History, 19th Century ; History, 20th Century ; Human Genome Project ; Humans ; Sequence Analysis, DNA
    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: 2001-10-27
    Description: Dendritic cells are involved in the initiation of both innate and adaptive immunity. To systematically explore how dendritic cells modulate the immune system in response to different pathogens, we used oligonucleotide microarrays to measure gene expression profiles of dendritic cells in response to Escherichia coli, Candida albicans, and influenza virus as well as to their molecular components. Both a shared core response and pathogen-specific programs of gene expression were observed upon exposure to each of these pathogens. These results reveal that dendritic cells sense diverse pathogens and elicit tailored pathogen-specific immune responses.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Huang, Q -- Liu, D -- Majewski, P -- Schulte, L C -- Korn, J M -- Young, R A -- Lander, E S -- Hacohen, N -- New York, N.Y. -- Science. 2001 Oct 26;294(5543):870-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Whitehead Institute for Biomedical Research, Cambridge, MA 02142, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11679675" target="_blank"〉PubMed〈/a〉
    Keywords: Antigen Presentation/genetics ; Candida albicans/*immunology ; Cells, Cultured ; Dendritic Cells/*immunology/metabolism ; Escherichia coli/*immunology ; Gene Expression Profiling ; *Gene Expression Regulation ; Humans ; Immunity, Innate ; Immunologic Factors/genetics ; Inflammation/immunology ; Influenza A virus/*immunology ; Leukocytes/immunology ; Lipopolysaccharides/immunology ; Mannans/immunology ; Oligonucleotide Array Sequence Analysis ; Phagocytosis ; RNA, Double-Stranded/immunology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 8
    Publication Date: 1999-10-16
    Description: Although cancer classification has improved over the past 30 years, there has been no general approach for identifying new cancer classes (class discovery) or for assigning tumors to known classes (class prediction). Here, a generic approach to cancer classification based on gene expression monitoring by DNA microarrays is described and applied to human acute leukemias as a test case. A class discovery procedure automatically discovered the distinction between acute myeloid leukemia (AML) and acute lymphoblastic leukemia (ALL) without previous knowledge of these classes. An automatically derived class predictor was able to determine the class of new leukemia cases. The results demonstrate the feasibility of cancer classification based solely on gene expression monitoring and suggest a general strategy for discovering and predicting cancer classes for other types of cancer, independent of previous biological knowledge.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Golub, T R -- Slonim, D K -- Tamayo, P -- Huard, C -- Gaasenbeek, M -- Mesirov, J P -- Coller, H -- Loh, M L -- Downing, J R -- Caligiuri, M A -- Bloomfield, C D -- Lander, E S -- New York, N.Y. -- Science. 1999 Oct 15;286(5439):531-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Whitehead Institute/Massachusetts Institute of Technology Center for Genome Research, Cambridge, MA 02139, USA. golub@genome.wi.mit.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10521349" target="_blank"〉PubMed〈/a〉
    Keywords: Acute Disease ; Antineoplastic Combined Chemotherapy Protocols/therapeutic use ; Cell Adhesion/genetics ; Cell Cycle/genetics ; *Gene Expression Profiling ; Homeodomain Proteins/genetics ; Humans ; Leukemia, Myeloid/*classification/drug therapy/*genetics ; Neoplasm Proteins/genetics ; Neoplasms/classification/genetics ; Oligonucleotide Array Sequence Analysis ; Oncogenes ; Precursor Cell Lymphoblastic Leukemia-Lymphoma/*classification/drug ; therapy/*genetics ; Predictive Value of Tests ; Reproducibility of Results ; Treatment Outcome
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 9
    Publication Date: 1998-06-06
    Description: Single-nucleotide polymorphisms (SNPs) are the most frequent type of variation in the human genome, and they provide powerful tools for a variety of medical genetic studies. In a large-scale survey for SNPs, 2.3 megabases of human genomic DNA was examined by a combination of gel-based sequencing and high-density variation-detection DNA chips. A total of 3241 candidate SNPs were identified. A genetic map was constructed showing the location of 2227 of these SNPs. Prototype genotyping chips were developed that allow simultaneous genotyping of 500 SNPs. The results provide a characterization of human diversity at the nucleotide level and demonstrate the feasibility of large-scale identification of human SNPs.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wang, D G -- Fan, J B -- Siao, C J -- Berno, A -- Young, P -- Sapolsky, R -- Ghandour, G -- Perkins, N -- Winchester, E -- Spencer, J -- Kruglyak, L -- Stein, L -- Hsie, L -- Topaloglou, T -- Hubbell, E -- Robinson, E -- Mittmann, M -- Morris, M S -- Shen, N -- Kilburn, D -- Rioux, J -- Nusbaum, C -- Rozen, S -- Hudson, T J -- Lipshutz, R -- Chee, M -- Lander, E S -- HG00098/HG/NHGRI NIH HHS/ -- HG01323/HG/NHGRI NIH HHS/ -- New York, N.Y. -- Science. 1998 May 15;280(5366):1077-82.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Whitehead Institute for Biomedical Research, Nine Cambridge Center, Cambridge, MA 02142, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9582121" target="_blank"〉PubMed〈/a〉
    Keywords: Algorithms ; Alleles ; Chromosome Mapping/*methods ; DNA, Complementary ; Databases, Factual ; Deoxyribonucleotides/*genetics ; Dinucleoside Phosphates ; Gene Expression ; Genetic Markers ; *Genetic Techniques ; Genetic Variation ; *Genome, Human ; *Genotype ; Heterozygote ; Homozygote ; Humans ; Molecular Sequence Data ; Nucleic Acid Hybridization ; Polymerase Chain Reaction ; *Polymorphism, Genetic ; Reproducibility of Results ; Sequence Analysis, DNA ; Sequence Tagged Sites
    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: 2010-02-19
    Description: A powerful way to discover key genes with causal roles in oncogenesis is to identify genomic regions that undergo frequent alteration in human cancers. Here we present high-resolution analyses of somatic copy-number alterations (SCNAs) from 3,131 cancer specimens, belonging largely to 26 histological types. We identify 158 regions of focal SCNA that are altered at significant frequency across several cancer types, of which 122 cannot be explained by the presence of a known cancer target gene located within these regions. Several gene families are enriched among these regions of focal SCNA, including the BCL2 family of apoptosis regulators and the NF-kappaBeta pathway. We show that cancer cells containing amplifications surrounding the MCL1 and BCL2L1 anti-apoptotic genes depend on the expression of these genes for survival. Finally, we demonstrate that a large majority of SCNAs identified in individual cancer types are present in several cancer types.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2826709/" 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/PMC2826709/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Beroukhim, Rameen -- Mermel, Craig H -- Porter, Dale -- Wei, Guo -- Raychaudhuri, Soumya -- Donovan, Jerry -- Barretina, Jordi -- Boehm, Jesse S -- Dobson, Jennifer -- Urashima, Mitsuyoshi -- Mc Henry, Kevin T -- Pinchback, Reid M -- Ligon, Azra H -- Cho, Yoon-Jae -- Haery, Leila -- Greulich, Heidi -- Reich, Michael -- Winckler, Wendy -- Lawrence, Michael S -- Weir, Barbara A -- Tanaka, Kumiko E -- Chiang, Derek Y -- Bass, Adam J -- Loo, Alice -- Hoffman, Carter -- Prensner, John -- Liefeld, Ted -- Gao, Qing -- Yecies, Derek -- Signoretti, Sabina -- Maher, Elizabeth -- Kaye, Frederic J -- Sasaki, Hidefumi -- Tepper, Joel E -- Fletcher, Jonathan A -- Tabernero, Josep -- Baselga, Jose -- Tsao, Ming-Sound -- Demichelis, Francesca -- Rubin, Mark A -- Janne, Pasi A -- Daly, Mark J -- Nucera, Carmelo -- Levine, Ross L -- Ebert, Benjamin L -- Gabriel, Stacey -- Rustgi, Anil K -- Antonescu, Cristina R -- Ladanyi, Marc -- Letai, Anthony -- Garraway, Levi A -- Loda, Massimo -- Beer, David G -- True, Lawrence D -- Okamoto, Aikou -- Pomeroy, Scott L -- Singer, Samuel -- Golub, Todd R -- Lander, Eric S -- Getz, Gad -- Sellers, William R -- Meyerson, Matthew -- K08 AR055688/AR/NIAMS NIH HHS/ -- K08 AR055688-03/AR/NIAMS NIH HHS/ -- K08 AR055688-04/AR/NIAMS NIH HHS/ -- K08 CA122833/CA/NCI NIH HHS/ -- K08 CA122833-01A1/CA/NCI NIH HHS/ -- K08 CA122833-02/CA/NCI NIH HHS/ -- K08 CA122833-03/CA/NCI NIH HHS/ -- K08 CA134931/CA/NCI NIH HHS/ -- K08CA122833/CA/NCI NIH HHS/ -- P01CA 098101/CA/NCI NIH HHS/ -- P01CA085859/CA/NCI NIH HHS/ -- P50CA90578/CA/NCI NIH HHS/ -- R01 CA109038/CA/NCI NIH HHS/ -- R01 GM074024/GM/NIGMS NIH HHS/ -- R01CA109038/CA/NCI NIH HHS/ -- R01CA109467/CA/NCI NIH HHS/ -- T32 GM007753/GM/NIGMS NIH HHS/ -- U24 CA126546/CA/NCI NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2010 Feb 18;463(7283):899-905. doi: 10.1038/nature08822.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cancer Program and Medical and Population Genetics Group, The Broad Institute of M.I.T. and Harvard, 7 Cambridge Center.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20164920" target="_blank"〉PubMed〈/a〉
    Keywords: Apoptosis/genetics ; Cell Line, Tumor ; Cell Survival/genetics ; DNA Copy Number Variations/*genetics ; Gene Amplification/genetics ; Gene Dosage/*genetics ; Genomics ; Humans ; Multigene Family/genetics ; Myeloid Cell Leukemia Sequence 1 Protein ; Neoplasms/classification/*genetics/pathology ; Proto-Oncogene Proteins c-bcl-2/genetics ; Signal Transduction ; bcl-X Protein/genetics
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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