Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Editorial
. 2023 Mar 21:14:216-218.
doi: 10.18632/oncotarget.28379.

Therapy drives genomic evolution in metastatic cancer

Ditte S Christensen, Nicolai J Birkbak
Editorial

Therapy drives genomic evolution in metastatic cancer

Ditte S Christensen et al. Oncotarget. .
No abstract available

Keywords: GENIE; cancer evolution; metastatic cancer mutations; treatment-induced mutations.

PubMed Disclaimer

Conflict of interest statement

CONFLICTS OF INTEREST

Authors have no conflicts of interest to declare.

Figures

Figure 1
Figure 1. Evolution of the metastatic cancer genome is dominated by clonal bottlenecking and anti-cancer treatment.
(A) Metastatic tumors are commonly observed as predominantly clonal, and with a general increase in tumor mutation burden and chromosomal instability relative to primary tumors. Abbreviations: TMB: Tumor mutation burden; CIN: Chromosomal instability; ITH: Intratumor heterogeneity. (B) Comparison of driver mutations in primary and metastatic tumors shows high consistency in the driver landscape, with only minor increases in aggressive cancer traits such as TP53 mutations and MYC amplifications observed in metastatic cancer. Only mutations associated with resistance, likely induced by anti-cancer therapy, are strongly enriched in metastatic cancer. (C) General model of metastatic cancer evolution. Created with http://BioRender.com.
See this image and copyright information in PMC

References

    1. Reiter JG, et al.. Nat Rev Cancer. 2019; 19:639–50. 10.1038/s41568-019-0185-x. - DOI - PMC - PubMed
    1. Hanahan D, et al.. Cell. 2011; 144:646–74. 10.1016/j.cell.2011.02.013. - DOI - PubMed
    1. Chaffer CL, et al.. Science. 2011; 331:1559–64. 10.1126/science.1203543. - DOI - PubMed
    1. Bailey MH, et al.. Cell. 2018; 173:371–85.e18. 10.1016/j.cell.2018.02.060. - DOI - PMC - PubMed
    1. Lawrence MS, et al.. Nature. 2014; 505:495–501. 10.1038/nature12912. - DOI - PMC - PubMed

Publication types