Genetic instability and death in cancer cells

Every time a cancer cell divides, it must copy its entire genome—and that process frequently goes wrong, creating breaks and tangles in the DNA that can either kill the cell or make it more dangerous. This project tackles a fundamental gap in knowledge: how cells respond to stress during DNA replication, and why those responses often fail in cancer. While scientists know that DNA damage triggers repair or cell death, the specific mechanisms at the replication fork—the molecular machinery that unwinds and copies DNA—remain poorly understood. Tumour cells routinely alter these pathways, which helps them survive and resist treatment. If this research succeeds, it could reveal new ways to push cancer cells into self-destruction by exploiting their own replication errors. That might lead to more effective chemotherapy or radiotherapy, or to drugs that selectively kill tumour cells while sparing healthy tissue. The work is fundamental science—it does not promise an immediate treatment. But similar studies of DNA repair pathways have already produced drugs such as PARP inhibitors, which now treat inherited breast and ovarian cancers. A deeper understanding of replication fork stress could open a comparable route for other cancers.