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  • 1
    Publication Date: 2001-03-28
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Roberts, R J -- Varmus, H E -- Ashburner, M -- Brown, P O -- Eisen, M B -- Khosla, C -- Kirschner, M -- Nusse, R -- Scott, M -- Wold, B -- New York, N.Y. -- Science. 2001 Mar 23;291(5512):2318-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉New England Biolabs, Beverly, MA 01915, USA. roberts@neb.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11269300" target="_blank"〉PubMed〈/a〉
    Keywords: *Archives ; Information Management ; *Information Services ; Information Storage and Retrieval ; *Internet ; National Institutes of Health (U.S.) ; *Periodicals as Topic ; *Publishing ; 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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  • 2
    Publication Date: 1999-04-24
    Description: T cell receptor (TCR) signaling requires activation of Zap-70 and Src family tyrosine kinases, but requirements for other tyrosine kinases are less clear. Combined deletion in mice of two Tec kinases, Rlk and Itk, caused marked defects in TCR responses including proliferation, cytokine production, and apoptosis in vitro and adaptive immune responses to Toxoplasma gondii in vivo. Molecular events immediately downstream from the TCR were intact in rlk-/-itk-/- cells, but intermediate events including inositol trisphosphate production, calcium mobilization, and mitogen-activated protein kinase activation were impaired, establishing Tec kinases as critical regulators of TCR signaling required for phospholipase C-gamma activation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schaeffer, E M -- Debnath, J -- Yap, G -- McVicar, D -- Liao, X C -- Littman, D R -- Sher, A -- Varmus, H E -- Lenardo, M J -- Schwartzberg, P L -- New York, N.Y. -- Science. 1999 Apr 23;284(5414):638-41.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉National Human Genome Research Institute, National Cancer Institute, National Institute for Allergy and Infectious Diseases, NIH, Bethesda, MD 20892, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10213685" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis ; CD4-CD8 Ratio ; Calcium Signaling ; Calcium-Calmodulin-Dependent Protein Kinases/metabolism ; Diglycerides/metabolism ; Gene Targeting ; Inositol Phosphates/metabolism ; Interferon-gamma/biosynthesis ; Interleukin-2/biosynthesis/pharmacology ; Isoenzymes/metabolism ; Killer Cells, Natural/immunology ; Lymphocyte Activation ; Mice ; Mutation ; Phospholipase C gamma ; Phosphorylation ; Protein-Tyrosine Kinases/genetics/*metabolism ; Receptors, Antigen, T-Cell/*metabolism ; *Signal Transduction ; T-Lymphocytes/*enzymology/*immunology ; Toxoplasmosis, Animal/immunology ; Type C Phospholipases/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
    Publication Date: 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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  • 4
    Publication Date: 1990-12-07
    Description: Virus envelope (Env) proteins are thought to contain specific signals for selective uptake by virus particles. In the course of attempting to define these signals by testing virus incorporation of CD4-Env chimeric proteins, normal human CD4 was found to be efficiently and selectively assembled into avian leukosis virus particles in quail cells. Viruses bearing CD4 at their surface may be useful reagents in the design of retrovirus-mediated gene therapy for the acquired immune deficiency syndrome.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Young, J A -- Bates, P -- Willert, K -- Varmus, H E -- New York, N.Y. -- Science. 1990 Dec 7;250(4986):1421-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Immunology, University of California School of Medicine, San Francisco 94143.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2175047" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD4/*genetics ; Avian Leukosis Virus/*genetics ; Cell Line ; Chimera ; Humans ; Quail ; Transfection ; Viral Envelope Proteins/*genetics ; Virion/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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  • 5
    Publication Date: 1984-06-08
    Description: A domain of DNA designated N-myc is amplified 20- to 140-fold in human neuroblastoma cell lines but not in cell lines from other tumor types. N-myc has now been found to be amplified in neuroblastoma tissue from 24 of 63 untreated patients (38 percent). The extent of amplification appears to be bimodal, with amplification of 100- to 300-fold in 12 cases and 3- to 10-fold in 10 others. Amplification was found in 0 of 15 patients with stage 1 or 2 disease, whereas 24 of 48 cases (50 percent) with stage 3 or 4 had evidence of N-myc amplification. These data indicate that N-myc amplification is a common event in untreated human neuroblastomas. Furthermore, N-myc amplification is highly correlated with advanced stages of disease (P less than 0.001) and with the ability to grow in vitro as an established cell line, both of which are associated with a poor prognosis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brodeur, G M -- Seeger, R C -- Schwab, M -- Varmus, H E -- Bishop, J M -- CA02971/CA/NCI NIH HHS/ -- CA13539/CA/NCI NIH HHS/ -- CA17829/CA/NCI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1984 Jun 8;224(4653):1121-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6719137" target="_blank"〉PubMed〈/a〉
    Keywords: Adolescent ; Adult ; Aged ; Cell Line ; Child ; Child, Preschool ; DNA, Neoplasm/genetics ; Eye Neoplasms/genetics ; *Gene Amplification ; Humans ; Infant ; Lymphatic Metastasis ; Middle Aged ; Neuroblastoma/*genetics/physiopathology ; Nucleic Acid Hybridization ; *Oncogenes ; Prognosis ; Retinoblastoma/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: 1982-05-21
    Description: Retroviruses have proved to be useful reagents for studying genetic and epigenetic (such as regulatory) changes in eukaryotic cells, for assessing functional and structural relationships between transposable genetic elements, for inducing insertional mutations, including some important in oncogenesis, and for transporting genes into eukaryotic cells, either after natural transduction of putative cellular oncogenes or after experimental construction of recombinant viruses. Many of these properties of retroviruses depend on their capacity to establish a DNA (proviral) form of their RNA genomes as a stable component of host chromosomes, in either somatic or germinal cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Varmus, H E -- New York, N.Y. -- Science. 1982 May 21;216(4548):812-20.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6177038" target="_blank"〉PubMed〈/a〉
    Keywords: Base Sequence ; DNA Transposable Elements ; DNA, Viral/biosynthesis/genetics ; Gene Expression Regulation ; Genes, Viral ; Genetic Vectors ; Mutation ; RNA-Directed DNA Polymerase/metabolism ; Recombination, Genetic ; Repetitive Sequences, Nucleic Acid ; Retroviridae/*physiology ; Transcription, Genetic ; Virus Replication
    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
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1987-12-04
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Varmus, H E -- New York, N.Y. -- Science. 1987 Dec 4;238(4832):1337-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology, University of California, San Francisco 94143.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2825348" target="_blank"〉PubMed〈/a〉
    Keywords: Avian Sarcoma Viruses/genetics ; Cell Transformation, Neoplastic/genetics ; DNA-Binding Proteins/genetics/physiology ; Fungal Proteins/genetics ; *Gene Expression Regulation ; Oncogene Protein p65(gag-jun) ; *Oncogenes ; *Protein Kinases ; Proto-Oncogene Proteins c-jun ; Retroviridae Proteins/genetics/physiology ; Saccharomyces cerevisiae/genetics ; *Saccharomyces cerevisiae Proteins ; Transcription Factors/genetics/physiology ; *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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  • 8
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1986-04-25
    Description: Hepatitis B viruses synthesize their open circular DNA genomes by reverse transcription of an RNA intermediate. The details of this process have been examined with the use of mammalian hepatitis B viruses to map the sites for initiation and termination of DNA synthesis and to explore the consequences of mutations introduced at short, separated direct repeats (DR1 and DR2) implicated in the mechanisms of initiation. The first DNA strand to be synthesized is initiated within DR1, apparently by a protein primer, and the completed strand has a short terminal redundancy. In contrast, the second DNA strand begins with the sequence adjacent to DR2, but its 5' end is joined to an oligoribonucleotide that contains DR1; thus the putative RNA primer has been transposed to the position of DR2. It is now possible to propose a detailed strategy for reverse transcription by hepatitis B viruses that can be instructively compared with that used by retroviruses.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Seeger, C -- Ganem, D -- Varmus, H E -- New York, N.Y. -- Science. 1986 Apr 25;232(4749):477-84.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3961490" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; DNA, Viral/metabolism ; Hepatitis B virus/genetics/*physiology ; Mutation ; RNA, Viral/metabolism ; Sciuridae ; Templates, Genetic ; *Virus Replication
    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: 1986-12-12
    Description: The presurface (preS) proteins of hepatitis B virus are structural components of the viral envelope that may play important roles in virion assembly and infectivity. They are specified by a large open reading frame that includes the coding region for the major surface (S) protein in its 3' half. Translation of the preS proteins initiates upstream from the S region, giving rise to proteins that are composed of the S domain and an additional 163 (preS1) or 55 (preS2) amino acids. Little is known about the biosynthesis and assembly of these proteins. The expression of the S and preS1 proteins was examined by transfecting cultured mammalian cells with viral DNA and injecting synthetic messenger RNA's into Xenopus oocytes. In contrast to the proteins encoded by the S region, the preS1 proteins are not detectably secreted into the culture medium. Furthermore, when the S and preS1 proteins are synthesized together, secretion of the S proteins is specifically and strongly inhibited. The results suggest a unique molecular interaction during secretion of the S and preS proteins that may be important for virus assembly.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Persing, D H -- Varmus, H E -- Ganem, D -- AI 18782/AI/NIAID NIH HHS/ -- GM07618/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1986 Dec 12;234(4782):1388-91.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3787251" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; DNA, Viral/administration & dosage ; Hepatitis B Surface Antigens/genetics/*pharmacology/*secretion ; Hepatitis B virus/genetics/pathogenicity ; Protein Biosynthesis ; Protein Precursors/genetics/*pharmacology ; Virion/pathogenicity ; Virus Replication ; Xenopus
    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
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1985-12-13
    Description: The pol gene of Rous sarcoma virus is positioned downstream of the gag gene in a different, briefly overlapping reading frame; nevertheless, the primary translation product of pol is a gag-pol fusion protein. Two mechanisms, ribosomal frameshifting and RNA splicing, have been considered to explain this phenomenon. The frameshifting model is supported by synthesis of both gag protein and gag-pol fusion protein in a cell-free mammalian translation system programmed by a single RNA species that was synthesized from cloned viral DNA with a bacteriophage RNA polymerase. Under these conditions, the ratio of the gag protein to the fusion protein (about 20 to 1) is similar to that previously observed in infected cells, the frameshifting is specific for the gag-pol junction, and it is unaffected by large deletions in gag. In addition, synthesis of the fusion protein is ten times less efficient in an Escherichia coli cell-free translation system and cannot be explained by transcriptional errors or in vitro modification of the RNA. Ribosomal frameshifting may affect production of other proteins in higher eukaryotes, including proteins encoded by several retroviruses and transposable elements.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jacks, T -- Varmus, H E -- New York, N.Y. -- Science. 1985 Dec 13;230(4731):1237-42.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2416054" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Avian Sarcoma Viruses/*genetics ; Base Sequence ; Cell-Free System ; *Gene Expression Regulation ; Gene Products, gag ; Molecular Weight ; *Protein Biosynthesis ; RNA, Messenger/genetics ; RNA, Viral/genetics ; RNA-Directed DNA Polymerase/*genetics ; Rabbits ; Retroviridae Proteins/genetics ; Ribosomes/*metabolism
    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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