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  • Signal Transduction  (34)
  • American Association for the Advancement of Science (AAAS)  (34)
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  • 1
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    Reovirus therapy of tumors with activated Ras pathway (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-11-13
    Description: Human reovirus requires an activated Ras signaling pathway for infection of cultured cells. To investigate whether this property can be exploited for cancer therapy, severe combined immune deficient mice bearing tumors established from v-erbB-transformed murine NIH 3T3 cells or human U87 glioblastoma cells were treated with the virus. A single intratumoral injection of virus resulted in regression of tumors in 65 to 80 percent of the mice. Treatment of immune-competent C3H mice bearing tumors established from ras-transformed C3H-10T1/2 cells also resulted in tumor regression, although a series of injections were required. These results suggest that, with further work, reovirus may have applicability in the treatment of cancer.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Coffey, M C -- Strong, J E -- Forsyth, P A -- Lee, P W -- New York, N.Y. -- Science. 1998 Nov 13;282(5392):1332-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cancer Biology Research Group and Department of Microbiology and Infectious Diseases, University of Calgary Health Science Centre, Calgary, Alberta, T2N 4N1, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9812900" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; Animals ; Antibodies, Viral/immunology ; Calcium-Calmodulin-Dependent Protein Kinases/metabolism ; Cell Line, Transformed ; Genes, erbB ; *Genes, ras ; Humans ; Male ; Mammalian orthoreovirus 3/immunology/*physiology ; Mice ; Mice, Inbred C3H ; Mice, SCID ; Neoplasm Transplantation ; Neoplasms, Experimental/metabolism/pathology/*therapy/virology ; Signal Transduction ; Tumor Cells, Cultured ; Virus Replication ; ras Proteins/*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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  • 2
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    Heterozygous germ line hCHK2 mutations in Li-Fraumeni syndrome (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-01-05
    Description: The hCHK2 gene encodes the human homolog of the yeast Cds1 and Rad53 G2 checkpoint kinases, whose activation in response to DNA damage prevents cellular entry into mitosis. Here, it is shown that heterozygous germ line mutations in hCHK2 occur in Li-Fraumeni syndrome, a highly penetrant familial cancer phenotype usually associated with inherited mutations in the TP53 gene. These observations suggest that hCHK2 is a tumor suppressor gene conferring predisposition to sarcoma, breast cancer, and brain tumors, and they also provide a link between the central role of p53 inactivation in human cancer and the well-defined G2 checkpoint in yeast.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bell, D W -- Varley, J M -- Szydlo, T E -- Kang, D H -- Wahrer, D C -- Shannon, K E -- Lubratovich, M -- Verselis, S J -- Isselbacher, K J -- Fraumeni, J F -- Birch, J M -- Li, F P -- Garber, J E -- Haber, D A -- New York, N.Y. -- Science. 1999 Dec 24;286(5449):2528-31.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Massachusetts General Hospital Center for Cancer Risk Analysis and Harvard Medical School, Building 149, Charlestown, MA 02129, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10617473" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Apoptosis ; Brain Neoplasms/genetics ; Breast Neoplasms/genetics ; Checkpoint Kinase 2 ; Female ; G1 Phase ; *G2 Phase ; *Genes, Tumor Suppressor ; Genes, p53 ; Genetic Predisposition to Disease ; *Germ-Line Mutation ; Heterozygote ; Humans ; Li-Fraumeni Syndrome/enzymology/*genetics/pathology ; Male ; Pedigree ; Polymorphism, Genetic ; Protein Kinases/genetics ; Protein-Serine-Threonine Kinases/*genetics/metabolism ; Sarcoma/genetics ; Signal Transduction ; Tumor Cells, Cultured
    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
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    Role of the S. typhimurium actin-binding protein SipA in bacterial internalization (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-03-26
    Description: Entry of the bacterium Salmonella typhimurium into host cells requires membrane ruffling and rearrangement of the actin cytoskeleton. Here, it is shown that the bacterial protein SipA plays a critical role in this process. SipA binds directly to actin, decreases its critical concentration, and inhibits depolymerization of actin filaments. These activities result in the spatial localization and more pronounced outward extension of the Salmonella-induced membrane ruffles, thereby facilitating bacterial uptake.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhou, D -- Mooseker, M S -- Galan, J E -- AI30492/AI/NIAID NIH HHS/ -- DK25387/DK/NIDDK NIH HHS/ -- GM52543/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1999 Mar 26;283(5410):2092-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Section of Microbial Pathogenesis, Boyer Center for Molecular Medicine, Yale School of Medicine, New Haven, CT 06536, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10092234" target="_blank"〉PubMed〈/a〉
    Keywords: Actins/chemistry/genetics/*metabolism ; Antigens, Bacterial/metabolism ; Bacterial Proteins/chemistry/genetics/*metabolism ; Binding Sites ; Biopolymers ; Cell Membrane/ultrastructure ; HeLa Cells ; Humans ; *Microfilament Proteins ; Microscopy, Fluorescence ; Mutation ; Recombinant Fusion Proteins/metabolism ; Salmonella typhimurium/genetics/metabolism/*pathogenicity ; Signal Transduction ; Vinculin/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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  • 4
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    Disruption of signaling by Yersinia effector YopJ, a ubiquitin-like protein protease (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-11-25
    Description: Homologs of the Yersinia virulence effector YopJ are found in both plant and animal bacterial pathogens, as well as plant symbionts. These YopJ family members were shown to act as cysteine proteases. The catalytic triad of the protease was required for inhibition of the mitogen-activated protein kinase (MAPK) and nuclear factor kappaB (NF-kappaB) signaling in animal cells and for induction of localized cell death in plants. The substrates for YopJ were shown to be highly conserved ubiquitin-like molecules, which are covalently added to numerous regulatory proteins. YopJ family members exert their pathogenic effect on cells by disrupting this posttranslational modification.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Orth, K -- Xu, Z -- Mudgett, M B -- Bao, Z Q -- Palmer, L E -- Bliska, J B -- Mangel, W F -- Staskawicz, B -- Dixon, J E -- 18024/PHS HHS/ -- AI41599/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2000 Nov 24;290(5496):1594-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Chemistry, University of Michigan, Ann Arbor, Michigan 48109-0606, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11090361" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Bacterial Proteins/*chemistry/genetics/*metabolism ; Catalysis ; Catalytic Domain ; Cell Line ; Cysteine Endopeptidases/chemistry/genetics/*metabolism ; Humans ; *MAP Kinase Signaling System ; Mitogen-Activated Protein Kinases/metabolism ; Molecular Sequence Data ; NF-kappa B/*metabolism ; Plant Leaves/cytology/virology ; SUMO-1 Protein ; Sequence Alignment ; Signal Transduction ; Transfection ; Ubiquitins/metabolism ; Virulence ; Xanthomonas campestris/enzymology/pathogenicity ; Yersinia pseudotuberculosis/enzymology/metabolism/*pathogenicity
    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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    Recruitment of a hedgehog regulatory circuit in butterfly eyespot evolution (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-01-23
    Description: The origin of new morphological characters is a long-standing problem in evolutionary biology. Novelties arise through changes in development, but the nature of these changes is largely unknown. In butterflies, eyespots have evolved as new pattern elements that develop from special organizers called foci. Formation of these foci is associated with novel expression patterns of the Hedgehog signaling protein, its receptor Patched, the transcription factor Cubitus interruptus, and the engrailed target gene that break the conserved compartmental restrictions on this regulatory circuit in insect wings. Redeployment of preexisting regulatory circuits may be a general mechanism underlying the evolution of novelties.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Keys, D N -- Lewis, D L -- Selegue, J E -- Pearson, B J -- Goodrich, L V -- Johnson, R L -- Gates, J -- Scott, M P -- Carroll, S B -- F32 GM18162/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 1999 Jan 22;283(5401):532-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and Laboratory of Molecular Biology, University of Wisconsin, 1525 Linden Drive, Madison, WI 53706, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9915699" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biological Evolution ; Body Patterning ; Butterflies/anatomy & histology/*genetics/growth & development ; DNA-Binding Proteins/genetics/physiology ; *Drosophila Proteins ; *Gene Expression Regulation ; Genes, Insect ; Hedgehog Proteins ; Homeodomain Proteins/genetics/physiology ; Insect Proteins/*genetics/physiology ; Membrane Proteins/genetics/physiology ; Pigmentation ; Receptors, Cell Surface ; Signal Transduction ; Transcription Factors/genetics/physiology ; Transcription, Genetic ; Wings, Animal/anatomy & histology/*growth & development/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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  • 6
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    Structure of the amino-terminal protein interaction domain of STAT-4 (1998)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1998-03-07
    Description: STATs (signal transducers and activators of transcription) are a family of transcription factors that are specifically activated to regulate gene transcription when cells encounter cytokines and growth factors. The crystal structure of an NH2-terminal conserved domain (N-domain) comprising the first 123 residues of STAT-4 was determined at 1.45 angstroms. The domain consists of eight helices that are assembled into a hook-like structure. The N-domain has been implicated in several protein-protein interactions affecting transcription, and it enables dimerized STAT molecules to polymerize and to bind DNA cooperatively. The structure shows that N-domains can interact through an extensive interface formed by polar interactions across one face of the hook. Mutagenesis of an invariant tryptophan residue at the heart of this interface abolished cooperative DNA binding by the full-length protein in vitro and reduced the transcriptional response after cytokine stimulation in vivo.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vinkemeier, U -- Moarefi, I -- Darnell, J E Jr -- Kuriyan, J -- AI32489/AI/NIAID NIH HHS/ -- AI34420/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1998 Feb 13;279(5353):1048-52.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular Cell Biology and Laboratories of Molecular Biophysics, The Rockefeller University, New York, NY 10021, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9461439" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Binding Sites ; Cell Line ; Crystallography, X-Ray ; DNA/metabolism ; DNA-Binding Proteins/*chemistry/genetics/metabolism ; Humans ; Hydrogen Bonding ; Interferon-gamma/pharmacology ; Models, Molecular ; Molecular Sequence Data ; Oligodeoxyribonucleotides/metabolism ; *Protein Conformation ; Protein Structure, Tertiary ; STAT1 Transcription Factor ; STAT4 Transcription Factor ; Signal Transduction ; Trans-Activators/*chemistry/genetics/metabolism ; Transcription, Genetic ; Transfection ; src Homology Domains
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
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  • 7
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    Specific expression of a tyrosine kinase gene, blk, in B lymphoid cells (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-01-19
    Description: Several pathways of transmembrane signaling in lymphocytes involve protein-tyrosine phosphorylation. With the exception of p56lck, a tyrosine kinase specific to T lymphoid cells that associates with the T cell transmembrane proteins CD4 and CD8, the kinases that function in these pathways are unknown. A murine lymphocyte complementary DNA that represents a new member of the src family has now been isolated and characterized. This complementary DNA, termed blk (for B lymphoid kinase), specifies a polypeptide of 55 kilodaltons that is related to, but distinct from, previously identified retroviral or cellular tyrosine kinases. The protein encoded by blk exhibits tyrosine kinase activity when expressed in bacterial cells. In the mouse and among cell lines, blk is specifically expressed in the B cell lineage. The tyrosine kinase encoded by blk may function in a signal transduction pathway that is restricted to B lymphoid cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dymecki, S M -- Niederhuber, J E -- Desiderio, S V -- New York, N.Y. -- Science. 1990 Jan 19;247(4940):332-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology and Genetics, Johns Hopkins University School of Medicine, Baltimore, MD 21205.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2404338" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; B-Lymphocytes/*enzymology ; Base Sequence ; Codon ; DNA/genetics/isolation & purification ; Escherichia coli/enzymology/genetics ; *Gene Expression ; Mice ; Molecular Sequence Data ; Protein-Tyrosine Kinases/*genetics ; Signal Transduction ; src-Family Kinases/*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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  • 8
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    Coactivation of receptor tyrosine kinases affects the response of tumor cells to targeted therapies (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-09-18
    Description: Targeted therapies that inhibit receptor tyrosine kinases (RTKs) and the downstream phosphatidylinositol 3-kinase (PI3K) signaling pathway have shown promising anticancer activity, but their efficacy in the brain tumor glioblastoma multiforme (GBM) and other solid tumors has been modest. We hypothesized that multiple RTKs are coactivated in these tumors and that redundant inputs drive and maintain downstream signaling, thereby limiting the efficacy of therapies targeting single RTKs. Tumor cell lines, xenotransplants, and primary tumors indeed show multiple concomitantly activated RTKs. Combinations of RTK inhibitors and/or RNA interference, but not single agents, decreased signaling, cell survival, and anchorage-independent growth even in glioma cells deficient in PTEN, a frequently inactivated inhibitor of PI3K. Thus, effective GBM therapy may require combined regimens targeting multiple RTKs.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stommel, Jayne M -- Kimmelman, Alec C -- Ying, Haoqiang -- Nabioullin, Roustem -- Ponugoti, Aditya H -- Wiedemeyer, Ruprecht -- Stegh, Alexander H -- Bradner, James E -- Ligon, Keith L -- Brennan, Cameron -- Chin, Lynda -- DePinho, Ronald A -- 5P01CA95616/CA/NCI NIH HHS/ -- R01CA99041/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2007 Oct 12;318(5848):287-90. Epub 2007 Sep 13.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medical Oncology, Dana-Farber Cancer Institute and Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17872411" target="_blank"〉PubMed〈/a〉
    Keywords: Antineoplastic Agents/*pharmacology ; Antineoplastic Combined Chemotherapy Protocols/pharmacology/therapeutic use ; Brain Neoplasms/drug therapy/*enzymology ; Cell Line, Tumor ; Cell Survival ; Enzyme Activation ; Erlotinib Hydrochloride ; Glioblastoma/drug therapy/*enzymology ; Humans ; Indoles/pharmacology ; PTEN Phosphohydrolase/genetics/metabolism ; Phosphatidylinositol 3-Kinases/metabolism ; Phosphorylation ; Piperazines/pharmacology ; Protein Kinase Inhibitors/*pharmacology ; Proto-Oncogene Proteins/metabolism ; Proto-Oncogene Proteins c-met ; Quinazolines/pharmacology ; Receptor Protein-Tyrosine Kinases/antagonists & inhibitors/*metabolism ; Receptor, Epidermal Growth Factor/antagonists & inhibitors/metabolism ; Receptors, Growth Factor/metabolism ; Signal Transduction ; Sulfonamides/pharmacology
    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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    Amyloid-beta dynamics are regulated by orexin and the sleep-wake cycle (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-09-26
    Description: Amyloid-beta (Abeta) accumulation in the brain extracellular space is a hallmark of Alzheimer's disease. The factors regulating this process are only partly understood. Abeta aggregation is a concentration-dependent process that is likely responsive to changes in brain interstitial fluid (ISF) levels of Abeta. Using in vivo microdialysis in mice, we found that the amount of ISF Abeta correlated with wakefulness. The amount of ISF Abeta also significantly increased during acute sleep deprivation and during orexin infusion, but decreased with infusion of a dual orexin receptor antagonist. Chronic sleep restriction significantly increased, and a dual orexin receptor antagonist decreased, Abeta plaque formation in amyloid precursor protein transgenic mice. Thus, the sleep-wake cycle and orexin may play a role in the pathogenesis of Alzheimer's disease.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2789838/" 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/PMC2789838/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kang, Jae-Eun -- Lim, Miranda M -- Bateman, Randall J -- Lee, James J -- Smyth, Liam P -- Cirrito, John R -- Fujiki, Nobuhiro -- Nishino, Seiji -- Holtzman, David M -- AG025824/AG/NIA NIH HHS/ -- AG029524/AG/NIA NIH HHS/ -- AG030946/AG/NIA NIH HHS/ -- K01 AG029524/AG/NIA NIH HHS/ -- K01 AG029524-03/AG/NIA NIH HHS/ -- K23 AG030946/AG/NIA NIH HHS/ -- K23 AG030946-03/AG/NIA NIH HHS/ -- MH072525/MH/NIMH NIH HHS/ -- NS065667/NS/NINDS NIH HHS/ -- P30 DK056341/DK/NIDDK NIH HHS/ -- P30 DK056341-09/DK/NIDDK NIH HHS/ -- P30 NS057105/NS/NINDS NIH HHS/ -- P30 NS057105-04/NS/NINDS NIH HHS/ -- P50 AG005681/AG/NIA NIH HHS/ -- R01 AG025824/AG/NIA NIH HHS/ -- R01 AG025824-03/AG/NIA NIH HHS/ -- R01 MH072525/MH/NIMH NIH HHS/ -- R01 MH072525-04/MH/NIMH NIH HHS/ -- R01 NS065667/NS/NINDS NIH HHS/ -- R01 NS065667-02/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2009 Nov 13;326(5955):1005-7. doi: 10.1126/science.1180962. Epub 2009 Sep 24.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurology, Washington University, St. Louis, MO 63110, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19779148" target="_blank"〉PubMed〈/a〉
    Keywords: Acetamides/pharmacology ; Alzheimer Disease/metabolism/*physiopathology ; Amyloid beta-Peptides/cerebrospinal fluid/*metabolism ; Animals ; Antigens, Surface/metabolism ; Circadian Rhythm ; Disease Models, Animal ; Extracellular Fluid/*metabolism ; Female ; Hippocampus/*metabolism ; Humans ; Intracellular Signaling Peptides and Proteins/administration & dosage/*metabolism ; Isoquinolines/pharmacology ; Light ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Neuropeptides/administration & dosage/*metabolism ; Orexin Receptors ; Orexins ; Receptors, Cell Surface/metabolism ; Receptors, G-Protein-Coupled/metabolism ; Receptors, Neuropeptide/metabolism ; Signal Transduction ; *Sleep ; Sleep Deprivation ; *Wakefulness
    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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    The genetic landscape of the childhood cancer medulloblastoma (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-12-18
    Description: Medulloblastoma (MB) is the most common malignant brain tumor of children. To identify the genetic alterations in this tumor type, we searched for copy number alterations using high-density microarrays and sequenced all known protein-coding genes and microRNA genes using Sanger sequencing in a set of 22 MBs. We found that, on average, each tumor had 11 gene alterations, fewer by a factor of 5 to 10 than in the adult solid tumors that have been sequenced to date. In addition to alterations in the Hedgehog and Wnt pathways, our analysis led to the discovery of genes not previously known to be altered in MBs. Most notably, inactivating mutations of the histone-lysine N-methyltransferase genes MLL2 or MLL3 were identified in 16% of MB patients. These results demonstrate key differences between the genetic landscapes of adult and childhood cancers, highlight dysregulation of developmental pathways as an important mechanism underlying MBs, and identify a role for a specific type of histone methylation in human tumorigenesis.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3110744/" 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/PMC3110744/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Parsons, D Williams -- Li, Meng -- Zhang, Xiaosong -- Jones, Sian -- Leary, Rebecca J -- Lin, Jimmy Cheng-Ho -- Boca, Simina M -- Carter, Hannah -- Samayoa, Josue -- Bettegowda, Chetan -- Gallia, Gary L -- Jallo, George I -- Binder, Zev A -- Nikolsky, Yuri -- Hartigan, James -- Smith, Doug R -- Gerhard, Daniela S -- Fults, Daniel W -- VandenBerg, Scott -- Berger, Mitchel S -- Marie, Suely Kazue Nagahashi -- Shinjo, Sueli Mieko Oba -- Clara, Carlos -- Phillips, Peter C -- Minturn, Jane E -- Biegel, Jaclyn A -- Judkins, Alexander R -- Resnick, Adam C -- Storm, Phillip B -- Curran, Tom -- He, Yiping -- Rasheed, B Ahmed -- Friedman, Henry S -- Keir, Stephen T -- McLendon, Roger -- Northcott, Paul A -- Taylor, Michael D -- Burger, Peter C -- Riggins, Gregory J -- Karchin, Rachel -- Parmigiani, Giovanni -- Bigner, Darell D -- Yan, Hai -- Papadopoulos, Nick -- Vogelstein, Bert -- Kinzler, Kenneth W -- Velculescu, Victor E -- CA057345/CA/NCI NIH HHS/ -- CA096832/CA/NCI NIH HHS/ -- CA118822/CA/NCI NIH HHS/ -- CA121113/CA/NCI NIH HHS/ -- CA135877/CA/NCI NIH HHS/ -- GM074906-01A1/GM/NIGMS NIH HHS/ -- HHSN261200800001E/PHS HHS/ -- P01 CA096832/CA/NCI NIH HHS/ -- P01 CA096832-03/CA/NCI NIH HHS/ -- R01 CA108622/CA/NCI NIH HHS/ -- R01 CA121113/CA/NCI NIH HHS/ -- R01 CA121113-05/CA/NCI NIH HHS/ -- R37 CA057345/CA/NCI NIH HHS/ -- R37 CA057345-20/CA/NCI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2011 Jan 28;331(6016):435-9. doi: 10.1126/science.1198056. Epub 2010 Dec 16.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Ludwig Center for Cancer Genetics and Therapeutics and Howard Hughes Medical Institute, Johns Hopkins Kimmel Cancer Center, Baltimore, MD 21231, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21163964" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Cerebellar Neoplasms/*genetics/metabolism ; Child ; DNA Copy Number Variations ; DNA-Binding Proteins/genetics/metabolism ; *Genes, Neoplasm ; Genes, Tumor Suppressor ; Histone-Lysine N-Methyltransferase/genetics/metabolism ; Histones/metabolism ; Humans ; Medulloblastoma/*genetics/metabolism ; Methylation ; MicroRNAs/genetics ; *Mutation ; Neoplasm Proteins/genetics/metabolism ; Oligonucleotide Array Sequence Analysis ; Point Mutation ; Sequence Analysis, DNA ; Signal Transduction
    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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