DNA Damage Can Persists for Years
Long-lived DNA damage in stem cells persists for years, raising cancer risks by amplifying harmful mutations.

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Researchers at the Wellcome Sanger Institute have uncovered a surprising form of DNA damage that persists for years without repair, posing risks for generating harmful mutations. The findings shed light on how these persistent damages may contribute to cancer by introducing multiple mutations over time.
DNA damage and its distinction from mutations
DNA damage and mutations are different phenomena. Mutations involve errors in the genetic sequence, such as the incorrect placement of one of the four DNA bases (A, G, T, or C). In contrast, DNA damage is a chemical alteration of the DNA, making it difficult for the sequence to be accurately read and replicated. During cell division, unrepaired DNA damage can lead to replication errors, introducing mutations into the genome.
Somatic mutation
A genetic alteration acquired by a cell that can be passed to its descendants through cell division. These mutations are not inherited but occur in somatic cells throughout an individual’s lifetime.
DNA replication
The biological process by which a cell duplicates its DNA before cell division. Errors during replication can lead to mutations.
Cells possess repair mechanisms to fix most DNA damage, but the study found that certain forms of damage evade these mechanisms. This damage persists through multiple cell divisions, increasing the likelihood of harmful mutations that can lead to cancer.
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Subscribe for FREEAnalyzing cellular family trees to uncover mutation patterns
The research team analyzed family trees of single cells from various tissues, including blood stem cells, bronchial epithelial cells, and liver cells. By studying patterns of shared mutations, they traced back cellular relationships and inferred mutation origins. The dataset included 103 somatic phylogenies from 89 individuals, providing comprehensive insights into mutation inheritance.
Somatic phylogeny
A "family tree" of cells, constructed based on shared mutations, used to study the history of cell divisions and mutation accumulation.
Their analysis revealed that between 15–20% of mutations in blood stem cells arose from a specific type of persistent DNA damage. This form of damage was found to last for an average of two to three years and occasionally longer.
Implications for cancer development
The persistence of DNA damage over time allows multiple opportunities for replication errors during cell division. Each error introduces a distinct mutation, amplifying the risk of cancer development. While rare, this long-lived damage can result in as many mutations as more common forms of DNA damage.
Interestingly, this phenomenon was predominantly observed in blood stem cells, raising questions about why similar processes are not seen in other healthy tissues. The findings suggest a tissue-specific mechanism underlying the persistence of certain DNA damages.
Advancing our understanding of mutations
This research challenges previous assumptions about how mutations accumulate and highlights the need for further studies into the causes and mechanisms of DNA damage. Understanding these processes may eventually lead to strategies for mitigating mutation risks and preventing associated diseases, including cancer.
Reference: Spencer Chapman M, Mitchell E, Yoshida K, et al. Prolonged persistence of mutagenic DNA lesions in somatic cells. Nature. 2025. doi: 10.1038/s41586-024-08423-8
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