Skip to main content

Thank you for visiting nature.com. You are using a browser version with limited support for CSS. To obtain the best experience, we recommend you use a more up to date browser (or turn off compatibility mode in Internet Explorer). In the meantime, to ensure continued support, we are displaying the site without styles and JavaScript.

Stem cells

Dual response to Ras mutation

Nature volume 504, pages 91–92 (2013)Cite this article

Subjects

Proliferation-driving mutations in haematopoietic stem cells often result in the loss of stem-cell properties. But at least one common oncogenic mutation seems to enhance both proliferation and stem-cell self-renewal. See Letter p.143

When a stem cell divides, it can either produce differentiated cells or self-renew to produce more stem cells. Because stem cells are thought to be the cells of origin for many types of cancer, understanding what controls this decision has become a central question in stem-cell and cancer research. During the formation of mature blood cells from haematopoietic stem cells (HSCs), these processes are often diametrically opposed: blood cells are produced through a hierarchical process of proliferation and differentiation, often at the expense of the stem-cell ability to self-renew. But how is this decision altered when a stem cell acquires a cancer-driving mutation? Previous studies have shown that mutations that increase the proliferation of HSCs tend to reduce the cells' potential for self-renewal. But on page 143 of this issue, Li et al.1 report that HSCs harbouring an activating mutation of the protein Nras show not only enhanced proliferation but also enhanced self-renewal.

This is a preview of subscription content, access via your institution

Access options

Rent or buy this article

Get just this article for as long as you need it

$39.95

Learn more

Prices may be subject to local taxes which are calculated during checkout

Figure 1: Bimodal behaviour.

References

  1. Li, Q. et al. Nature 504, 143–147 (2013).

    Article  ADS  CAS  Google Scholar 

  2. Wang, J. et al. Blood 121, 5203–5207 (2013).

    Article  CAS  Google Scholar 

  3. Kotecha, N. et al. Cancer Cell 14, 335–343 (2008).

    Article  CAS  Google Scholar 

  4. Chang, T. et al. J. Clin. Invest. 123, 335–339 (2013).

    Article  CAS  Google Scholar 

  5. Wilson, A. et al. Cell 135, 1118–1129 (2008).

    Article  CAS  Google Scholar 

  6. Dykstra, B. et al. Cell Stem Cell 1, 218–229 (2007).

    Article  CAS  Google Scholar 

  7. Yamamoto, R. et al. Cell 154, 1112–1126 (2013).

    Article  CAS  Google Scholar 

  8. Sabnis, A. J. et al. PLoS Biol. 7, e1000059 (2009).

    Article  Google Scholar 

  9. Li, Q. et al. Blood 117, 2022–2032 (2011).

    Article  CAS  Google Scholar 

  10. Wang, Y. et al. Science 327, 1650–1653 (2010).

    Article  ADS  CAS  Google Scholar 

  11. Friedmann-Morvinski, D. et al. Science 338, 1080–1084 (2012).

    Article  ADS  CAS  Google Scholar 

Download references

Author information

Authors and Affiliations

  1. S. Haihua Chu and Scott A. Armstrong are at the Memorial Sloan-Kettering Cancer Center, New York, New York 10065, USA.,

    S. Haihua Chu & Scott A. Armstrong

Authors
  1. S. Haihua Chu
    View author publications

    You can also search for this author in PubMed Google Scholar

  2. Scott A. Armstrong
    View author publications

    You can also search for this author in PubMed Google Scholar

Corresponding author

Correspondence to Scott A. Armstrong.

Rights and permissions

Reprints and Permissions

About this article

Cite this article

Chu, S., Armstrong, S. Dual response to Ras mutation. Nature 504, 91–92 (2013). https://doi.org/10.1038/nature12840

Download citation

  • Published:

  • Issue Date:

  • DOI: https://doi.org/10.1038/nature12840

Search

Advanced search

Quick links

Nature Briefing: Cancer

Sign up for the Nature Briefing: Cancer newsletter — what matters in cancer research, free to your inbox weekly.

Get what matters in cancer research, free to your inbox weekly. Sign up for Nature Briefing: Cancer