Genomic instability is a hallmark of cancer, and it often arises from defective DNA replication. When the replication fork is not adequately protected, it can collapse or stall, leading to incomplete DNA replication and the accumulation of mutations. These mutations can activate oncogenes or inactivate tumor suppressor genes, driving the transformation of normal cells into cancerous cells. Therefore, understanding and enhancing fork protection can be crucial in developing cancer therapies.
