A 2026 study in Nature reports that cancer-associated circular DNA has fragile repeating regions and may depend on repair proteins to survive damage. The findings point to a possible way to destabilize some tumours, but they are preclinical research—not evidence of a new cancer treatment for patients.
What is circular DNA in cancer?
Extrachromosomal DNA, or ecDNA, is genetic material that forms circles outside a cell’s chromosomes. It can carry amplified cancer-driving genes, helping tumour cells maintain extra copies of genes that promote growth. The 2026 paper by David Billing and colleagues estimates that ecDNA is found in approximately 17% of human cancers; that is a prevalence estimate, not a measure of treatment response or survival (Billing et al., Nature, 23 September 2026).
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How could ecDNA become a weakness?
Billing and colleagues report that TA-rich repeating DNA regions on ecDNA are prone to breaks. The study examined these sites and ecDNA maintenance through laboratory experiments, including work in COLO320DM cancer cells, alongside analyses of tumour genomic data. Rearrangement breakpoints were enriched at TA-rich regions, and the resulting structural changes included deletions and small duplications.
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Two repair steps help protect ecDNA
The authors describe two parts of the cells’ response to this damage. FANCM reduces break formation at TA-rich sites. When breaks persist, the ERCC1–ERCC4 complex can cleave them, and polymerase theta (Polθ) can help repair some through microhomology-mediated end joining (MMEJ).
When researchers depleted FANCM or inhibited Polθ in experimental cancer cells, ecDNA damage and structural rearrangements increased. This suggests that ecDNA maintenance may depend on these repair functions. It does not mean all circular DNA is easily destroyed: the reported vulnerability is tied to particular DNA sequences and cellular repair machinery.
Could this lead to a cancer treatment?
The authors propose that inhibiting Polθ might destabilize ecDNA and make ecDNA-driven tumours more susceptible to treatment. Their conclusion is a potential therapeutic direction, not proof that this strategy works in people (Billing et al., Nature, 23 September 2026; see also Watson and Korbel, Nature News & Views, 6 October 2026).
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The cited sources do not establish clinical benefit, safety or efficacy in patients, show which patients might respond, or demonstrate that a Polθ inhibitor is available as a cancer treatment. The findings do not justify changing or stopping treatment. They describe a mechanism supported by laboratory and genomic research, with further work needed to determine whether it can become a safe and effective therapy.
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DNA breaks and repair can generate rearrangements. The same instability that researchers hope to exploit may therefore also contribute to the ongoing evolution of tumours. The study’s therapeutic idea is not simply to “destroy” ecDNA; it is to investigate whether disrupting repair can make ecDNA less stable in a way that helps treatment, without assuming that the consequences are straightforward.
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Disclosure relevant to the therapeutic idea
The primary paper reports that senior author Agnel Sfeir is a co-founder, consultant and shareholder of Repare Therapeutics, and that several other listed authors are current or former company employees (Billing et al., Nature, 23 September 2026). This disclosure is relevant context when considering the paper’s proposed translational direction; it does not by itself determine whether the findings are valid.
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