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Oncogene-induced senescence is part of the tumorigenesis barrier imposed by DNA damage checkpoints

Author

Listed:
  • Jirina Bartkova

    (Institute of Cancer Biology and Centre for Genotoxic Stress Research, Danish Cancer Society)

  • Nousin Rezaei

    (The Wistar Institute)

  • Michalis Liontos

    (School of Medicine, University of Athens)

  • Panagiotis Karakaidos

    (School of Medicine, University of Athens)

  • Dimitris Kletsas

    (Institute of Biology, Demokritos National Center for Scientific Research)

  • Natalia Issaeva

    (Microbiology and Toxicology, Stockholm University)

  • Leandros-Vassilios F. Vassiliou

    (School of Medicine, University of Athens)

  • Evangelos Kolettas

    (School of Medicine, University of Ioannina)

  • Katerina Niforou

    (School of Medicine, University of Athens)

  • Vassilis C. Zoumpourlis

    (Institute of Biological Research and Biotechnology, National Hellenic Research Foundation)

  • Munenori Takaoka

    (University of Pennsylvania)

  • Hiroshi Nakagawa

    (University of Pennsylvania)

  • Frederic Tort

    (Institute of Cancer Biology and Centre for Genotoxic Stress Research, Danish Cancer Society)

  • Kasper Fugger

    (Institute of Cancer Biology and Centre for Genotoxic Stress Research, Danish Cancer Society)

  • Fredrik Johansson

    (Microbiology and Toxicology, Stockholm University)

  • Maxwell Sehested

    (University Hospital)

  • Claus L. Andersen

    (Aarhus University Hospital)

  • Lars Dyrskjot

    (Aarhus University Hospital)

  • Torben Ørntoft

    (Aarhus University Hospital)

  • Jiri Lukas

    (Institute of Cancer Biology and Centre for Genotoxic Stress Research, Danish Cancer Society)

  • Christos Kittas

    (School of Medicine, University of Athens)

  • Thomas Helleday

    (Microbiology and Toxicology, Stockholm University
    University of Sheffield)

  • Thanos D. Halazonetis

    (The Wistar Institute
    University of Geneva)

  • Jiri Bartek

    (Institute of Cancer Biology and Centre for Genotoxic Stress Research, Danish Cancer Society)

  • Vassilis G. Gorgoulis

    (School of Medicine, University of Athens)

Abstract

Cancer and cell senescence Cancer is commonly thought of as uncontrolled cellular proliferation, but in the early stages of many cancers, oncogene expression is associated with cellular senescence. A possible explanation for this has now been found. Two groups report a link between oncogene-induced senescence and the DNA damage response. Activated oncogenes can cause aberrant DNA replication and thereby DNA damage that can lead to cell senescence. Cellular senescence was found previously to be a barrier to tumorigenesis in vivo, so oncogene-induced senescence may be an innate defence against cancer. But its effectiveness is often disabled by further mutations. Understanding the relationship between cell senescence and tumour formation may aid in the development of diagnostic and prognostic tools based on senescence markers.

Suggested Citation

  • Jirina Bartkova & Nousin Rezaei & Michalis Liontos & Panagiotis Karakaidos & Dimitris Kletsas & Natalia Issaeva & Leandros-Vassilios F. Vassiliou & Evangelos Kolettas & Katerina Niforou & Vassilis C. , 2006. "Oncogene-induced senescence is part of the tumorigenesis barrier imposed by DNA damage checkpoints," Nature, Nature, vol. 444(7119), pages 633-637, November.
    • Handle: RePEc:nat:nature:v:444:y:2006:i:7119:d:10.1038_nature05268
    DOI: 10.1038/nature05268
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    Cited by:

    1. Jianbang Wang & Zhenzhen Li & Itamar Willner, 2022. "Cascaded dissipative DNAzyme-driven layered networks guide transient replication of coded-strands as gene models," Nature Communications, Nature, vol. 13(1), pages 1-10, December.
    2. Taichi Igarashi & Marianne Mazevet & Takaaki Yasuhara & Kimiyoshi Yano & Akifumi Mochizuki & Makoto Nishino & Tatsuya Yoshida & Yukihiro Yoshida & Nobuhiko Takamatsu & Akihide Yoshimi & Kouya Shiraish, 2023. "An ATR-PrimPol pathway confers tolerance to oncogenic KRAS-induced and heterochromatin-associated replication stress," Nature Communications, Nature, vol. 14(1), pages 1-22, December.
    3. Karl-Uwe Reusswig & Julia Bittmann & Martina Peritore & Mathilde Courtes & Benjamin Pardo & Michael Wierer & Matthias Mann & Boris Pfander, 2022. "Unscheduled DNA replication in G1 causes genome instability and damage signatures indicative of replication collisions," Nature Communications, Nature, vol. 13(1), pages 1-20, December.
    4. Karl-Heinz Tomaszowski & Sunetra Roy & Carolina Guerrero & Poojan Shukla & Caezaan Keshvani & Yue Chen & Martina Ott & Xiaogang Wu & Jianhua Zhang & Courtney D. DiNardo & Detlev Schindler & Katharina , 2023. "Hypomorphic Brca2 and Rad51c double mutant mice display Fanconi anemia, cancer and polygenic replication stress," Nature Communications, Nature, vol. 14(1), pages 1-15, December.
    5. Hervé Técher & Diyavarshini Gopaul & Jonathan Heuzé & Nail Bouzalmad & Baptiste Leray & Audrey Vernet & Clément Mettling & Jérôme Moreaux & Philippe Pasero & Yea-Lih Lin, 2024. "MRE11 and TREX1 control senescence by coordinating replication stress and interferon signaling," Nature Communications, Nature, vol. 15(1), pages 1-14, December.
    6. Sascha Schäuble & Karolin Klement & Shiva Marthandan & Sandra Münch & Ines Heiland & Stefan Schuster & Peter Hemmerich & Stephan Diekmann, 2012. "Quantitative Model of Cell Cycle Arrest and Cellular Senescence in Primary Human Fibroblasts," PLOS ONE, Public Library of Science, vol. 7(8), pages 1-14, August.

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