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  • 1
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    Comment on "A global map of human impact on marine ecosystems" (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-09-13
    Description: Halpern et al. (Reports, 15 February 2008, p. 948) integrated spatial data on 17 drivers of change in the oceans to map the global distribution of human impact. Although fishery catches are a dominant driver, the data reflect activity while impacts occur at different space and time scales. Failure to account for this spatial disconnection could lead to potentially misleading conclusions.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Heath, Michael R -- New York, N.Y. -- Science. 2008 Sep 12;321(5895):1446; author reply 1446. doi: 10.1126/science.1157390.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Fisheries Research Services, Marine Laboratory, 375 Victoria Road, Aberdeen AB11 9DB, UK. heathmr@marlab.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18787153" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Ecosystem ; *Fisheries ; *Fishes ; Food Chain ; *Human Activities ; Humans ; Oceans and Seas ; Population Dynamics
    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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  • 2
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    Systems biology and new technologies enable predictive and preventative medicine (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-10-23
    Description: Systems approaches to disease are grounded in the idea that disease-perturbed protein and gene regulatory networks differ from their normal counterparts; we have been pursuing the possibility that these differences may be reflected by multiparameter measurements of the blood. Such concepts are transforming current diagnostic and therapeutic approaches to medicine and, together with new technologies, will enable a predictive and preventive medicine that will lead to personalized medicine.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hood, Leroy -- Heath, James R -- Phelps, Michael E -- Lin, Biaoyang -- New York, N.Y. -- Science. 2004 Oct 22;306(5696):640-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Systems Biology, Seattle, WA, USA. lhood@systemsbiology.org〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15499008" target="_blank"〉PubMed〈/a〉
    Keywords: Biomarkers/blood ; *Computational Biology ; Databases, Nucleic Acid ; Diagnosis ; *Disease ; Disease Progression ; Forecasting ; Gene Expression ; Gene Expression Profiling ; Gene Expression Regulation, Neoplastic ; Humans ; Male ; Microfluidics ; Nanotechnology ; *Preventive Medicine ; Prostate/physiology ; Prostatic Neoplasms/genetics/metabolism ; Systems Analysis ; Systems Theory ; Therapeutics
    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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  • 3
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    Targeted therapy resistance mediated by dynamic regulation of extrachromosomal mutant EGFR DNA (2013)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2013-12-07
    Description: Intratumoral heterogeneity contributes to cancer drug resistance, but the underlying mechanisms are not understood. Single-cell analyses of patient-derived models and clinical samples from glioblastoma patients treated with epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs) demonstrate that tumor cells reversibly up-regulate or suppress mutant EGFR expression, conferring distinct cellular phenotypes to reach an optimal equilibrium for growth. Resistance to EGFR TKIs is shown to occur by elimination of mutant EGFR from extrachromosomal DNA. After drug withdrawal, reemergence of clonal EGFR mutations on extrachromosomal DNA follows. These results indicate a highly specific, dynamic, and adaptive route by which cancers can evade therapies that target oncogenes maintained on extrachromosomal DNA.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4049335/" 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/PMC4049335/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nathanson, David A -- Gini, Beatrice -- Mottahedeh, Jack -- Visnyei, Koppany -- Koga, Tomoyuki -- Gomez, German -- Eskin, Ascia -- Hwang, Kiwook -- Wang, Jun -- Masui, Kenta -- Paucar, Andres -- Yang, Huijun -- Ohashi, Minori -- Zhu, Shaojun -- Wykosky, Jill -- Reed, Rachel -- Nelson, Stanley F -- Cloughesy, Timothy F -- James, C David -- Rao, P Nagesh -- Kornblum, Harley I -- Heath, James R -- Cavenee, Webster K -- Furnari, Frank B -- Mischel, Paul S -- NS73831/NS/NINDS NIH HHS/ -- P01 CA095616/CA/NCI NIH HHS/ -- P01-CA95616/CA/NCI NIH HHS/ -- P30 CA023100/CA/NCI NIH HHS/ -- R01 NS052563/NS/NINDS NIH HHS/ -- R01 NS073831/NS/NINDS NIH HHS/ -- R01 NS080939/NS/NINDS NIH HHS/ -- R01-NS080939/NS/NINDS NIH HHS/ -- T32 CA009056/CA/NCI NIH HHS/ -- U54 CA151819/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2014 Jan 3;343(6166):72-6. doi: 10.1126/science.1241328. Epub 2013 Dec 5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Ludwig Institute for Cancer Research, University of California at San Diego, La Jolla, CA, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24310612" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antineoplastic Agents/*therapeutic use ; Central Nervous System Neoplasms/*drug therapy/genetics ; DNA/genetics ; Drug Resistance, Neoplasm/*genetics ; Erlotinib Hydrochloride ; Glioblastoma/*drug therapy/genetics ; Humans ; Mice ; *Molecular Targeted Therapy ; Mutation ; Neoplasm Transplantation ; Protein Kinase Inhibitors/*therapeutic use ; Quinazolines/therapeutic use ; Receptor, Epidermal Growth Factor/antagonists & inhibitors/*genetics ; Single-Cell Analysis ; Tumor Cells, Cultured ; Withholding Treatment
    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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