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Mad2-induced chromosome instability leads to lung tumour relapse after oncogene withdrawal

Author

Listed:
  • Rocio Sotillo

    (Cancer Biology and Genetics Program,)

  • Juan-Manuel Schvartzman

    (Cancer Biology and Genetics Program,)

  • Nicholas D. Socci

    (Computational Biology Center, Memorial Sloan-Kettering Cancer Center, New York, New York 10065, USA)

  • Robert Benezra

    (Cancer Biology and Genetics Program,)

Abstract

Double jeopardy from genomic instability Genomic instability has been implicated in tumorigenesis. In a new mouse model for Kras-driven lung tumours in which genomic instability is caused by overexpression of the spindle checkpoint protein Mad2, Sotillo et al. find that switching off the Kras oncogene still leads to cancer regression, but tumours recur at a much higher rate. This suggests that genomic instability not only promotes tumorigenesis but may also contribute to recurrences after cancer therapy and possibly to therapeutic resistance.

Suggested Citation

  • Rocio Sotillo & Juan-Manuel Schvartzman & Nicholas D. Socci & Robert Benezra, 2010. "Mad2-induced chromosome instability leads to lung tumour relapse after oncogene withdrawal," Nature, Nature, vol. 464(7287), pages 436-440, March.
    • Handle: RePEc:nat:nature:v:464:y:2010:i:7287:d:10.1038_nature08803
    DOI: 10.1038/nature08803
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    Cited by:

    1. Wei-Yi Cheng & Tai-Hsien Ou Yang & Dimitris Anastassiou, 2013. "Biomolecular Events in Cancer Revealed by Attractor Metagenes," PLOS Computational Biology, Public Library of Science, vol. 9(2), pages 1-14, February.

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