科技科学

Circular DNA exposes a weakness in cancer cells

Nature正文已收录本站
  • NEWS AND VIEWS

Repetitive sequences make extrachromosomal DNA vulnerable to breaks, which could be exploited for therapy — but might also promote tumour evolution.

By

  1. Nikolaus A. Watson

    1. Nikolaus A. Watson is in the Genome Biology Unit at the European Molecular Biology Laboratory, 69117 Heidelberg, Germany.

  2. Jan O. Korbel

    1. Jan O. Korbel is in the Genome Biology Unit at the European Molecular Biology Laboratory, 69117 Heidelberg, Germany, and in the Bridging Research Division on Mechanisms of Genomic Variation and Data Science at the German Cancer Research Center, Heidelberg, Germany.

Cancer genomes are always changing. The genetic alterations that initiate and promote tumour growth can create conditions for genome evolution1, which enables cancer cells to acquire properties over time through a phenomenon known as genomic instability. Understanding what enables such evolutionary flexibility is central to explaining how tumour cells adapt. It could also inform the development of cancer treatments. Writing in Nature, Billing et al.2 examine a form of genetic material that often arises in genomically unstable tumours: circular, non-chromosomal DNA known as extrachromosomal DNA (ecDNA)3.

Nature 658, 324-325 (2026)

doi: https://doi.org/10.1038/d41586-026-02966-8

References

  1. Cosenza, M. R., Rodriguez-Martin, B. & Korbel, J. O. Annu. Rev. Genom. Hum. Genet. 23, 123–152 (2022).

    Article  Google Scholar 

  2. Billing, D. et al. Nature 658, 525–535 (2026).

    Article  Google Scholar 

  3. Wu, S., Bafna, V., Chang, H. Y. & Mischel, P. S. Annu. Rev. Pathol. Mech. Dis. 17, 367–386 (2022).

    Article  Google Scholar 

  4. Wu, S. et al. Nature 575, 699–703 (2019).

    Article  PubMed  Google Scholar 

  5. Sfeir, A., Tijsterman, M. & McVey, M. Annu. Rev. Cell Dev. Biol. 40, 195–218 (2024).

    Article  PubMed  Google Scholar 

  6. Kang, X. et al. Cell 188, 3405–3421 (2025).

    Article  PubMed  Google Scholar 

  7. Tang, J. et al. Nature 635, 210–218 (2024).

    Article  PubMed  Google Scholar 

  8. Rosswog, C. et al. Nature Genet. 53, 1673–1685 (2021).

    Article  PubMed  Google Scholar 

  9. Cosenza, M. R. et al. Nature 648, 383–393 (2025).

    Article  PubMed  Google Scholar 

  10. Umbreit, N. T. et al. Science 368, eaba0712 (2020).

    Article  PubMed  Google Scholar 

  11. Shoshani, O. et al. Nature 591, 137–141 (2021).

    Article  PubMed  Google Scholar 

Download references

Competing Interests

The authors declare no competing interests.

Related Articles

  • Read the paper: MMEJ repair of breaks at TA repeats maintains ecDNA and cancer fitness

  • Circular DNA has a ticket to ride chromosomes

  • Extrachromosomal DNA appears before cancer forms

  • See all News & Views

Subjects

Latest on:

  • Cancer
  • Molecular biology

  • Can pancreatic cancer be stopped in its tracks? Radical tactic raises hopes

    News

  • Osteoclasts intercept meningeal lymphatic paths for dural metastasis

    Article

  • Pipework problems when cancer spreads to an area bordering the brain

    News & Views

  • Histone readers MLLT1 and MLLT3 concentrate AID to confer locus specificity

    Article

  • Transcription pause and elongation regulators mediate somatic hypermutation

    Article

  • Surprising protein links dietary restriction to increased lifespan in flies

    News & Views