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A dynamic view of chemotherapy effectiveness

Chemotherapy can halt cancer by causing cells to enter a non-dividing state called senescence, but sometimes it causes tumour cells to proliferate. It now seems that the dynamics of the protein p21 governs which of these fates occurs.
  1. Yunpeng Liu

    1. Yunpeng Liu is at the Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139, USA.

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  2. Michael T. Hemann

    1. Michael T. Hemann is at the Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139, USA.

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Chemotherapy usually works by inducing DNA damage that leads to cell death. However, rather than dying after chemotherapy, some tumour cells enter an inactive state, termed senescence, in which they are alive but have permanently stopped dividing1. Although senescence in normal cells drives ageing and tissue degeneration2, cancer-therapy-induced senescence is associated with positive clinical outcomes3. Understanding the factors that drive the senescence of tumour cells might thus aid the development of new anticancer treatments. Writing in Cell, Hsu et al.4 shed light on a previously unknown aspect of how chemotherapy-induced entry into senescence is controlled.

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Nature 572, 321-322 (2019)

doi: https://doi.org/10.1038/d41586-019-02336-7

References

  1. Campisi, J. & d’Adda di Fagagna, F. Nature Rev. Mol. Cell Biol. 8, 729–740 (2007).

    Article  PubMed  Google Scholar 

  2. Campisi, J. Annu. Rev. Physiol. 75, 685–705 (2013).

    Article  PubMed  Google Scholar 

  3. Ewald, J. A., Desotelle, J. A., Wilding, G. & Jarrard, D. F. J. Natl Cancer Inst. 102, 1536–1546 (2010).

    Article  PubMed  Google Scholar 

  4. Hsu, C.-H., Altschuler, S. J. & Wu, L. F. Cell 178, 361–373 (2019).

    Article  PubMed  Google Scholar 

  5. d’Adda di Fagagna, F. Nature Rev. Cancer 8, 512–522 (2008).

    Article  PubMed  Google Scholar 

  6. Fitzgerald, A. L. et al. Cell Death Dis. 6, e1678 (2015).

    Article  PubMed  Google Scholar 

  7. Abbas, T. & Dutta, A. Nature Rev. Cancer 9, 400–414 (2009).

    Article  PubMed  Google Scholar 

  8. Potter, A. J. et al. Carcinogenesis 23, 389–401 (2002).

    Article  PubMed  Google Scholar 

Download references

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