21.3.18 General

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10 thoughts on “21.3.18 General”

  1. Genome-wide CRISPR-Cas9 Screen Identifies Leukemia-Specific Dependence on a Pre-mRNA Metabolic Pathway Regulated by DCPS

    Takuji Yamauchi, Takeshi Masuda, Matthew C. Canver, Michael Seiler, Yuichiro Semba, Mohammad Shboul, Mohammed Al-Raqad, Manami Maeda, Vivien A.C. Schoonenberg, Mitchel A. Cole, Claudio Macias-Trevino, Yuichi Ishikawa, Qiuming Yao, Michitaka Nakano, Fumio Arai, Stuart H. Orkin, Bruno Reversade, Silvia Buonamici, Luca Pinello, Koichi Akashi, Daniel E. Bauer, Takahiro Maeda11,’Correspondence information about the author Takahiro Maeda

    http://www.cell.com/cancer-cell/abstract/S1535-6108(18)30012-6

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  2. http://science.sciencemag.org.libproxy.helsinki.fi/content/359/6378/920

    Patient-derived organoids model treatment response of metastatic gastrointestinal cancers

    Georgios Vlachogiannis1, Somaieh Hedayat1, Alexandra Vatsiou2, Yann Jamin3, Javier Fernández-Mateos1,2, Khurum Khan1,4, Andrea Lampis1, Katherine Eason1, Ian Huntingford1, Rosemary Burke5, Mihaela Rata3, Dow-Mu Koh3,6, Nina Tunariu3,6, David Collins3, Sanna Hulkki-Wilson1, Chanthirika Ragulan1, Inmaculada Spiteri2, Sing Yu Moorcraft4, Ian Chau4, Sheela Rao4, David Watkins4, Nicos Fotiadis6, Maria Bali3,6, Mahnaz Darvish-Damavandi1, Hazel Lote1,4, Zakaria Eltahir1, Elizabeth C. Smyth4, Ruwaida Begum4, Paul A. Clarke5, Jens C. Hahne1, Mitchell Dowsett7, Johann de Bono8, Paul Workman5, Anguraj Sadanandam1, Matteo Fassan9, Owen J. Sansom10, Suzanne Eccles5, Naureen Starling4, Chiara Braconi4,5, Andrea Sottoriva2, Simon P. Robinson3, David Cunningham4, Nicola Valeri1,4,*

    1Division of Molecular Pathology, The Institute of Cancer Research, London, UK.
    2Centre for Evolution and Cancer, The Institute of Cancer Research, London, UK.
    3Cancer Research UK Cancer Imaging Centre, Division of Radiotherapy and Imaging, The Institute of Cancer Research and Royal Marsden Hospital, London, UK.
    4Department of Medicine, The Royal Marsden NHS Trust, London, UK.
    5Cancer Research UK Cancer Therapeutics Unit, The Institute of Cancer Research, London, UK.
    6Department of Radiology, The Royal Marsden NHS Trust, London, UK.
    7Ralph Lauren Centre for Breast Cancer Research, Royal Marsden Hospital NHS Trust, London, UK.
    8Division of Clinical Studies, The Institute of Cancer Research, London, UK.
    9Department of Medicine, Surgical Pathology and Cytopathology Unit, University of Padua, Padua, Italy.
    10Cancer Research UK Beatson Institute, Glasgow, UK.

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  3. BRD4 Inhibition Is Synthetic Lethal with PARP Inhibitors through the Induction of Homologous Recombination Deficiency
    Chaoyang Sun10,’Correspondence information about the author Chaoyang SunEmail the author Chaoyang Sun, Jun Yin, Yong Fang, Jian Chen, Kang Jin Jeong, Xiaohua Chen, Christopher P. Vellano, Zhenlin Ju, Wei Zhao, Dong Zhang, Yiling Lu, Funda Meric-Bernstam, Timothy A. Yap, Maureen Hattersley, Mark J. O’Connor, Huawei Chen, Stephen Fawell, Shiaw-Yih Lin, Guang Peng, Gordon B. Mills

    http://www.cell.com/cancer-cell/fulltext/S1535-6108(18)30019-9

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  4. Resolvins suppress tumor growth and enhance cancer therapy

    Megan L. Sulciner, View ORCID ProfileCharles N. Serhan Correspondence email, View ORCID ProfileMolly M. Gilligan, Dayna K. Mudge, Jaimie Chang, Allison Gartung, Kristen A. Lehner, Diane R. Bielenberg, Birgitta Schmidt, Jesmond Dalli, Emily R. Greene, Yael Gus-Brautbar, Julia Piwowarski, Tadanori Mammoto, David Zurakowski, View ORCID ProfileMauro Perretti, Vikas P. Sukhatme, Arja Kaipainen, View ORCID ProfileMark W. Kieran Correspondence email, Sui Huang Correspondence email, Dipak Panigrahy

    http://jem.rupress.org/content/215/1/115.long

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  5. TEM8/ANTXR1-Specific CAR T Cells as a Targeted Therapy for Triple-Negative Breast Cancer

    Tiara T. Byrd, Kristen Fousek, Antonella Pignata, Christopher Szot, Heba Samaha, Steven Seaman, Lacey Dobrolecki, Vita S. Salsman, Htoo Zarni Oo, Kevin Bielamowicz, Daniel Landi, Nino Rainusso, John Hicks, Suzanne Powell, Matthew L. Baker, Winfried S. Wels, Joachim Koch, Poul H. Sorensen, Benjamin Deneen, Matthew J. Ellis, Michael T. Lewis, Meenakshi Hegde, Bradley S. Fletcher, Brad St. Croix and Nabil Ahmed

    http://cancerres.aacrjournals.org.libproxy.helsinki.fi/content/78/2/489

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  6. Genes Dev. 2018 Feb 1;32(3-4):230-243. doi: 10.1101/gad.309062.117. Epub 2018 Feb 20.
    Mutant p53 controls tumor metabolism and metastasis by regulating PGC-1α.
    Basu S1, Gnanapradeepan K1,2, Barnoud T1, Kung CP1, Tavecchio M3, Scott J1, Watters A3, Chen Q3, Kossenkov AV4, Murphy ME1.
    Author information
    Abstract

    Mutant forms of p53 protein often possess protumorigenic functions, conferring increased survival and migration to tumor cells via their “gain-of-function” activity. Whether and how a common polymorphism in TP53 at amino acid 72 (Pro72Arg; referred to here as P72 and R72) impacts this gain of function has not been determined. We show that mutant p53 enhances migration and metastasis of tumors through the ability to bind and regulate PGC-1α and that this regulation is markedly impacted by the codon 72 polymorphism. Tumor cells with the R72 variant of mutant p53 show increased PGC-1α function along with greatly increased mitochondrial function and metastatic capability. Breast cancers containing mutant p53 and the R72 variant show poorer prognosis compared with P72. The combined results reveal PGC-1α as a novel “gain-of-function” partner of mutant p53 and indicate that the codon 72 polymorphism influences the impact of mutant p53 on metabolism and metastasis.

    http://genesdev.cshlp.org/content/early/2018/02/19/gad.309062.117.full.pdf+html

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