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  • 1
    Publication Date: 2014-06-12
    Description: Inhibitors against the p110delta isoform of phosphoinositide-3-OH kinase (PI(3)K) have shown remarkable therapeutic efficacy in some human leukaemias. As p110delta is primarily expressed in leukocytes, drugs against p110delta have not been considered for the treatment of solid tumours. Here we report that p110delta inactivation in mice protects against a broad range of cancers, including non-haematological solid tumours. We demonstrate that p110delta inactivation in regulatory T cells unleashes CD8(+) cytotoxic T cells and induces tumour regression. Thus, p110delta inhibitors can break tumour-induced immune tolerance and should be considered for wider use in oncology.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4501086/" 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/PMC4501086/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ali, Khaled -- Soond, Dalya R -- Pineiro, Roberto -- Hagemann, Thorsten -- Pearce, Wayne -- Lim, Ee Lyn -- Bouabe, Hicham -- Scudamore, Cheryl L -- Hancox, Timothy -- Maecker, Heather -- Friedman, Lori -- Turner, Martin -- Okkenhaug, Klaus -- Vanhaesebroeck, Bart -- 095691/Wellcome Trust/United Kingdom -- 095691/Z/11/Z/Wellcome Trust/United Kingdom -- 12888/Cancer Research UK/United Kingdom -- 14355/Cancer Research UK/United Kingdom -- A10200/Cancer Research UK/United Kingdom -- A12888/Cancer Research UK/United Kingdom -- A15965/Cancer Research UK/United Kingdom -- BB/E009867/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- C18270/A12888/Cancer Research UK/United Kingdom -- C23338/A10200/Cancer Research UK/United Kingdom -- C23338/A15965/Cancer Research UK/United Kingdom -- England -- Nature. 2014 Jun 19;510(7505):407-11. doi: 10.1038/nature13444. Epub 2014 Jun 11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] UCL Cancer Institute, Paul O'Gorman Building, University College London, 72 Huntley Street London WC1E 6DD, UK [2]. ; 1] Laboratory of Lymphocyte Signalling and Development, The Babraham Institute, Babraham Research Campus, Cambridge CB22 3AT, UK [2] [3]. ; Centre for Cancer and Inflammation, Barts Cancer Institute, Queen Mary University of London, Charterhouse Square, London EC1M 6BQ, UK. ; UCL Cancer Institute, Paul O'Gorman Building, University College London, 72 Huntley Street London WC1E 6DD, UK. ; Laboratory of Lymphocyte Signalling and Development, The Babraham Institute, Babraham Research Campus, Cambridge CB22 3AT, UK. ; Mary Lyon Centre, MRC Harwell, Harwell Science and Innovation Campus, Harwell OX11 0RD, UK. ; Piramed Pharma, 957 Buckingham Avenue, Slough, Berkshire SL1 4NL, UK. ; Cancer Signaling and Translational Oncology, Genentech Inc, 1 DNA Way, South San Francisco, California 94080-4990, USA. ; 1] Laboratory of Lymphocyte Signalling and Development, The Babraham Institute, Babraham Research Campus, Cambridge CB22 3AT, UK [2].〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24919154" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antineoplastic Agents/pharmacology ; Enzyme Activation/drug effects ; Enzyme Inhibitors/*pharmacology ; Immune Tolerance/*drug effects/immunology ; Mice ; Neoplasms/*enzymology/*immunology ; Phosphatidylinositol 3-Kinases/*metabolism ; T-Lymphocytes, Regulatory/*drug effects/enzymology/immunology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 2
    Publication Date: 2015-09-25
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pearce-Higgins, James W -- England -- Nature. 2015 Sep 24;525(7570):455. doi: 10.1038/525455b.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉British Trust for Ornithology, Thetford, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26399822" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Birds ; *Conflict of Interest ; Cost-Benefit Analysis ; Data Collection ; Great Britain ; *Hobbies ; Motivation ; *Research Design ; Science/*manpower ; *Volunteers/psychology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 3
    Publication Date: 2016-03-05
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pearce, Warren -- Hartley, Sarah -- Nerlich, Brigitte -- England -- Nature. 2016 Mar 3;531(7592):35. doi: 10.1038/531035d.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉University of Nottingham, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26935688" target="_blank"〉PubMed〈/a〉
    Keywords: Humans ; *Information Dissemination ; Research/*standards
    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: 2016-04-07
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ali, Khaled -- Soond, Dalya R -- Pineiro, Roberto -- Hagemann, Thorsten -- Pearce, Wayne -- Lim, Ee Lyn -- Bouabe, Hicham -- Scudamore, Cheryl L -- Hancox, Timothy -- Maecker, Heather -- Friedman, Lori -- Turner, Martin -- Okkenhaug, Klaus -- Vanhaesebroeck, Bart -- Nature. 2016 Apr 6. doi: 10.1038/nature17641.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27049952" target="_blank"〉PubMed〈/a〉
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 5
    Publication Date: 2008-05-02
    Description: Phosphoinositide 3-kinases (PI3Ks) signal downstream of multiple cell-surface receptor types. Class IA PI3K isoforms couple to tyrosine kinases and consist of a p110 catalytic subunit (p110alpha, p110beta or p110delta), constitutively bound to one of five distinct p85 regulatory subunits. PI3Ks have been implicated in angiogenesis, but little is known about potential selectivity among the PI3K isoforms and their mechanism of action in endothelial cells during angiogenesis in vivo. Here we show that only p110alpha activity is essential for vascular development. Ubiquitous or endothelial cell-specific inactivation of p110alpha led to embryonic lethality at mid-gestation because of severe defects in angiogenic sprouting and vascular remodelling. p110alpha exerts this critical endothelial cell-autonomous function by regulating endothelial cell migration through the small GTPase RhoA. p110alpha activity is particularly high in endothelial cells and preferentially induced by tyrosine kinase ligands (such as vascular endothelial growth factor (VEGF)-A). In contrast, p110beta in endothelial cells signals downstream of G-protein-coupled receptor (GPCR) ligands such as SDF-1alpha, whereas p110delta is expressed at low level and contributes only minimally to PI3K activity in endothelial cells. These results provide the first in vivo evidence for p110-isoform selectivity in endothelial PI3K signalling during angiogenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Graupera, Mariona -- Guillermet-Guibert, Julie -- Foukas, Lazaros C -- Phng, Li-Kun -- Cain, Robert J -- Salpekar, Ashreena -- Pearce, Wayne -- Meek, Stephen -- Millan, Jaime -- Cutillas, Pedro R -- Smith, Andrew J H -- Ridley, Anne J -- Ruhrberg, Christiana -- Gerhardt, Holger -- Vanhaesebroeck, Bart -- BB/C505659/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- BB/C505659/2/Biotechnology and Biological Sciences Research Council/United Kingdom -- G0601093/Medical Research Council/United Kingdom -- G0601093(79633)/Medical Research Council/United Kingdom -- G0700711/Medical Research Council/United Kingdom -- Cancer Research UK/United Kingdom -- England -- Nature. 2008 May 29;453(7195):662-6. doi: 10.1038/nature06892. Epub 2008 Apr 30.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Centre for Cell Signalling, Institute of Cancer, Queen Mary, University of London, Charterhouse Square, London EC1M 6BQ, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18449193" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Cell Movement ; Cells, Cultured ; Class I Phosphatidylinositol 3-Kinases ; Endothelial Cells/*cytology/*enzymology ; Female ; Humans ; Mice ; *Neovascularization, Physiologic ; Phosphatidylinositol 3-Kinases/genetics/*metabolism ; RNA Interference ; Rats ; Signal Transduction/drug effects ; Vascular Endothelial Growth Factor A/pharmacology ; Wounds and Injuries ; rho GTP-Binding Proteins/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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