Deletion of the TP53 gene, an event seen in colorectal cancers, often occurs with co-deletion of a gene that encodes an enzyme subunit governing gene transcription. This creates a vulnerability ripe for therapeutic development. See Letter p.697
This is a preview of subscription content, access via your institution
Access options
Subscribe to this journal
Receive 51 print issues and online access
$199.00 per year
only $3.90 per issue
Buy this article
- Purchase on Springer Link
- Instant access to full article PDF
Prices may be subject to local taxes which are calculated during checkout
Notes
References
Bryant, H. E. et al. Nature 434, 913–917 (2005).
Farmer, H. et al. Nature 434, 917–921 (2005).
Kandoth, C. et al. Nature 502, 333–339 (2013).
Liu, C. et al. Nature 520, 697–701 (2015).
Wade, M., Li, Y.-C. & Wahl, G. M. Nature Rev. Cancer 13, 83–96 (2013).
Muller, F. L. et al. Nature 488, 337–342 (2012).
Nijhawan, D. et al. Cell 150, 842–854 (2012).
Author information
Authors and Affiliations
Corresponding author
Rights and permissions
About this article
Cite this article
Bradner, J. An essential passenger with p53. Nature 520, 626–627 (2015). https://doi.org/10.1038/nature14390
Published:
Issue Date:
DOI: https://doi.org/10.1038/nature14390
This article is cited by
-
Knocking out matrix metalloproteinase 12 causes the accumulation of M2 macrophages in intestinal tumor microenvironment of mice
Cancer Immunology, Immunotherapy (2020)
