Tumor cells may fracture their own DNA while driving rapid growth
Researchers found that intense activity of cancer-driven super-enhancers can cause double-strand DNA breaks, which tumors repeatedly repair, fostering mutation accumulation.
Scientists at the Hebrew University of Jerusalem have mapped where the most severe DNA damage occurs in cancer genomes and discovered a concentration of double-strand breaks at super-enhancers, the DNA segments that amplify growth-related genes. The research, published in Science Advances, indicates that the relentless transcription driven by these regions physically strains the DNA, causing it to snap. Tumor cells repeatedly mend these lesions, but each repair cycle can insert minor mutations, gradually increasing genetic instability.
This process may help cancers evolve, acquire aggressiveness, or develop drug resistance. Because tumors depend on this high-stress DNA landscape, interfering with super-enhancer activity or the repair machinery could expose a vulnerability. The findings open a new avenue for therapies aimed at destabilizing the very drivers of tumor proliferation.
Why it matters
Understanding how cancer’s own growth mechanisms damage DNA reveals new targets for future treatments.
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