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MMEJ repair of breaks at TA repeats maintains ecDNA and cancer fitness

Research Cancer Genomics

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TL;DR - This Nature study links extrachromosomal DNA (ecDNA) stability in cancer to microhomology-mediated end joining at fragile TA-rich sites. Targeting Polθ may destabilize ecDNA and create a therapeutic vulnerability in ecDNA-driven tumours.

  • TA-rich sites are prone to breaks that threaten ecDNA maintenance.
  • Microhomology-mediated end joining repairs these breaks and preserves cancer fitness.
  • FANCM suppresses break formation at these fragile sites.
  • Disrupting Polθ-mediated repair could sensitize ecDNA-driven tumours to treatment.

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MMEJ repair of breaks at TA repeats maintains ecDNA and cancer fitness

Nature David Billing, Monica Selvaraj, Megan E. Kelley, Gabriel Matos-Rodrigues, Benton Bailey, Finnja Becker, Gang Zhen, Matthew A. Myers, Alessandra Brambati, Oluchi Ezekwenna, Ashley Nichols, Yi-Zhen Jiang, Lucia Wang, Shih-Chun Wang, Marie-Claude Mathieu, Davide Pradella, Hugo Poirier, Elias Rodriguez-Fos, Stephen J. Morris, Michal Zimmermann, Elsa Callen, Michael Zinda, Andrea Ventura, John Maciejowski, Andrew McPherson, Sohrab P. Shah, Anton George Henssen, André Nussenzweig, Agnel Sfeir 2026-09-23 doi:10.1038/s41586-026-11048-8
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Providers: Hugging Face · N/A OpenAlex · Citations 0 Publisher · N/A Semantic Scholar · Citations 0 · Influential citations 0 X · N/A Fetched 2026-09-26 14:13:51.928476 UTC

TL;DR - This Nature study links extrachromosomal DNA (ecDNA) stability in cancer to microhomology-mediated end joining at fragile TA-rich sites. Targeting Polθ may destabilize ecDNA and create a therapeutic vulnerability in ecDNA-driven tumours.

  • TA-rich sites are prone to breaks that threaten ecDNA maintenance.
  • Microhomology-mediated end joining repairs these breaks and preserves cancer fitness.
  • FANCM suppresses break formation at these fragile sites.
  • Disrupting Polθ-mediated repair could sensitize ecDNA-driven tumours to treatment.
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