Therapy-Induced Senescence: Opportunities to Improve Anticancer Therapy

DOI PDF PDF 被引用文献2件
  • Pataje G Prasanna
    National Cancer Institute, NIH , Bethesda, MD, USA
  • Deborah E Citrin
    National Cancer Institute, NIH , Bethesda, MD, USA
  • Jeffrey Hildesheim
    National Cancer Institute, NIH , Bethesda, MD, USA
  • Mansoor M Ahmed
    National Cancer Institute, NIH , Bethesda, MD, USA
  • Sundar Venkatachalam
    National Cancer Institute, NIH , Bethesda, MD, USA
  • Gabriela Riscuta
    National Cancer Institute, NIH , Bethesda, MD, USA
  • Dan Xi
    National Cancer Institute, NIH , Bethesda, MD, USA
  • Guangrong Zheng
    College of Pharmacy, University of Florida , Gainesville, FL, USA
  • Jan van Deursen
    Rochester , MN, USA
  • Jorg Goronzy
    Department of Medicine, Stanford University , Stanford, CA, USA
  • Stephen J Kron
    The University of Chicago , Chicago, IL, USA
  • Mitchell S Anscher
    U.S. Food and Drug Administration , Silver Spring, MD, USA
  • Norman E Sharpless
    National Cancer Institute, NIH , Bethesda, MD, USA
  • Judith Campisi
    Buck Institute for Research on Aging , Novato, CA, USA
  • Stephen L Brown
    Henry Ford Hospital , Detroit, MI, USA
  • Laura J Niedernhofer
    Institute on the Biology of Aging and Metabolism, Department of Biochemistry, Molecular Biology and Biophysics, University of Minnesota , Minneapolis, MN, USA
  • Ana O’Loghlen
    Epigenetics , 4 Newark Street , London, E1 2AT, UK
  • Alexandros G Georgakilas
    DNA Damage Laboratory, Physics Department, School of Applied Mathematical and Physical Sciences, National Technical University of Athens (NTUA) , Zografou , 15780, Athens, Greece
  • Francois Paris
    Universite de Nantes, INSERM, CNRS, CRCINA , Nantes, France
  • David Gius
    University of Texas Health Sciences Center , San Antonio, San Antonio, TX, USA
  • David A Gewirtz
    Virginia Commonwealth University , Richmond, VA, USA
  • Clemens A Schmitt
    Charité - Universitätsmedizin , 13353, Berlin, Germany
  • Mohamed E Abazeed
    Johannes Kepler University , 4020, Linz, Austria
  • James L Kirkland
    Robert and Arlene Kogod Center on Aging, Mayo Clinic , Rochester, MN, USA
  • Ann Richmond
    Department of Pharmacology and Department of Veterans Affairs, Vanderbilt University , Nashville, TN, USA
  • Paul B Romesser
    Translational Research Division, Department of Radiation Oncology and Early Drug Development Service, Department of Medicine, Memorial Hospital, Memorial Sloan Kettering Cancer Center , New York, NY, USA
  • Scott W Lowe
    Cancer Biology and Genetics Program, Sloan Kettering Institute, Memorial Sloan Kettering Cancer Center, and Howard Hughes Medical Institute , New York, NY, USA
  • Jesus Gil
    MRC London Institute of Medical Sciences (LMS), and Institute of Clinical Sciences, Faculty of Medicine, Imperial College London , Du Cane Road , London, W12 ONN, UK
  • Marc S Mendonca
    Departments of Radiation Oncology & Medical and Molecular Genetics, Indiana University School of Medicine, IUPUI , Indianapolis, IN 46202, USA
  • Sandeep Burma
    Departments of Neurosurgery and Biochemistry & Structural Biology, University of Texas Health Science Center , San Antonio, TX, USA
  • Daohong Zhou
    College of Pharmacy, University of Florida , Gainesville, FL, USA
  • C Norman Coleman
    National Cancer Institute, NIH , Bethesda, MD, USA

抄録

<jats:title>Abstract</jats:title> <jats:p>Cellular senescence is an essential tumor suppressive mechanism that prevents the propagation of oncogenically activated, genetically unstable, and/or damaged cells. Induction of tumor cell senescence is also one of the underlying mechanisms by which cancer therapies exert antitumor activity. However, an increasing body of evidence from preclinical studies demonstrates that radiation and chemotherapy cause accumulation of senescent cells (SnCs) both in tumor and normal tissue. SnCs in tumors can, paradoxically, promote tumor relapse, metastasis, and resistance to therapy, in part, through expression of the senescence-associated secretory phenotype. In addition, SnCs in normal tissue can contribute to certain radiation- and chemotherapy-induced side effects. Because of its multiple roles, cellular senescence could serve as an important target in the fight against cancer. This commentary provides a summary of the discussion at the National Cancer Institute Workshop on Radiation, Senescence, and Cancer (August 10-11, 2020, National Cancer Institute, Bethesda, MD) regarding the current status of senescence research, heterogeneity of therapy-induced senescence, current status of senotherapeutics and molecular biomarkers, a concept of “one-two punch” cancer therapy (consisting of therapeutics to induce tumor cell senescence followed by selective clearance of SnCs), and its integration with personalized adaptive tumor therapy. It also identifies key knowledge gaps and outlines future directions in this emerging field to improve treatment outcomes for cancer patients.</jats:p>

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