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Our bodies consist of trillions of cells that constantly divide and renew. During this process, the DNA in each cell must be copied and distributed accurately. Sometimes, DNA becomes damaged, for example by radiation or chemotherapy. Double-strand DNA breaks are particularly dangerous. If not properly repaired, they can lead to DNA errors, cell death or cancer.

Fortunately, cells have multiple ways to repair DNA. Two key repair routes are NHEJ (fast but error-prone) and HR (slower but more precise). With modern techniques like CRISPR/Cas9, we can intentionally cause breaks and study how cells respond. Our research shows that the location of the CRISPR/Cas9 break in the genome has little impact on how harmful the break is.

We also found that the MND1 protein plays an important role in accurate repair. Without this protein, cells switch to less precise repair methods. Additionally, the presence of the tumor suppressor protein p53 determines which repair pathway is chosen. If p53 is absent, cells more often use error-prone methods, which can promote cancer development.

Finally, the research shows that cancer cells with disrupted signaling pathways are vulnerable to drug combinations that further stress their DNA. By exploiting these weaknesses, new therapies can be developed.