The Double Face of Base Excision Repair: Preventing and Triggering Double-Strand Breaks.
Level 5 - mechanism / opinion, no new human data
Narrative review of molecular mechanisms without original human data
PubMed 41273051 · doi:10.1002/bies.70092
What was done
This is a narrative review synthesizing literature on how base excision repair (BER) machinery responds to oxidative DNA damage and the mechanisms through which it either repairs DNA or induces secondary damage.
What was found
The abstract reports no numerical data or statistical findings. It notes qualitatively that while BER typically replaces oxidized bases to restore the DNA double helix, it can under specific circumstances generate double-strand breaks, provoke chromosome fragmentation, and lead to genomic rearrangements correlated with oncogenesis. These outcomes are modulated by damage type, lesion clustering, repair pathway selection, and chromatin remodelers.
Why it matters
It clarifies the dual role of a fundamental DNA repair mechanism, detailing how aberrant base excision repair can paradoxically drive genomic instability and oncogenesis.
Limits
The abstract describes a narrative review without primary empirical data, quantitative effect estimates, sample sizes, or a systematic literature search methodology.
Cited by
- supports Every cell in the human body experiences at least one broken chromosome every day, amounting to approximately 20 trillion chromosome breakage events daily across the body.