Research suggests that cancer cells may be evolving by damaging their own DNA.

It has been suggested that cancer cells may overactivate genes necessary for proliferation, resulting in severe damage to their own DNA, and that errors during repair may lead to the accumulation of new mutations. It has been pointed out that some of this DNA damage is caused by cancer cells overactivating genes necessary for proliferation, and that this may lead to tumor changes and adaptation to treatment.

Superenhancers shape the landscape and repair dynamics of transcription-associated DNA breaks in cancer | Science Advances

https://www.science.org/doi/10.1126/sciadv.aeb6379

Cancer may be breaking its own DNA to keep growing | ScienceDaily
https://www.sciencedaily.com/releases/2026/07/260731034204.htm

The process of reading genetic information and creating RNA is called 'transcription.' In normal cells, the strength of transcription is regulated for each gene, but cancer cells excessively transcribe some genes related to proliferation. When transcriptional activity becomes too high, it puts transcriptional stress on the DNA, which can lead to 'DNA double-strand breaks,' where both strands that make up the DNA break. DNA double-strand breaks are a particularly serious type of DNA damage.

Osama Hidmi of Hebrew University of Jerusalem and cancer researcher Professor Rami Akeyran identified the locations of DNA double-strand breaks across the entire genome and compared them with gene transcription levels and markers involved in DNA repair. Their findings revealed that DNA damage was not evenly distributed throughout the genome, but concentrated within genes controlled by 'super-enhancers,' which are DNA regions that strongly stimulate nearby genes. In these genes, not only was DNA breakage actively occurring, but repair was also actively taking place.

It is thought that genes regulated by super-enhancers experience increased transcriptional activity, making them more susceptible to DNA double-strand breaks. Since DNA double-strand breaks can lead to cell death if repair fails, they are dangerous damage to individual cancer cells. On the other hand, cells that repair their DNA and survive may retain mutations. If some of these mutations are advantageous for proliferation and survival, those cells will grow within the tumor.

According to the research team, regions where DNA is repeatedly cut and repaired are weak points for cancer cells, but they can also be sources of mutations that give cancer new properties. They suggest that properties such as resistance to treatment or the spread of cancer to other tissues may also arise from similar processes in the long term.

The research team states that the excessive gene activity and DNA repair mechanisms induced by super-enhancers may become potential therapeutic targets in the future. They added that further investigation is needed to determine whether this will lead to future treatments.