Genome instability serves as a defining characteristic of cancer. Throughout the process of DNA replication, various obstacles can impede the progression of replication forks, arising from both cellular metabolic processes and environmental factors. These impediments have the potential to disrupt the normal course of replication and pose a threat to genome stability. In response, cells have developed a diverse range of mechanisms to counteract replication fork stalling and rescue stalled replication, thereby safeguarding the integrity of the genome. An in-depth understanding of these protective mechanisms holds significant implications for unraveling the early events in the development of cancer.

Moreover, recent research has shed light on the potential of targeting replication processes in tumor cells as a promising therapeutic approach for cancer treatment, particularly in cases where cancer cells harbor mutations in DNA repair genes. This emerging therapeutic strategy takes advantage of the vulnerabilities of tumor cells and their increased reliance on replication mechanisms, offering a novel avenue for intervention. By selectively disrupting or impairing the replication processes within cancer cells, it becomes possible to induce damage to their DNA, ultimately inhibiting their growth and proliferation.

To gain insights into the molecular mechanisms underlying the preservation of genome stability under replication stress, our Lab employs a multidisciplinary approach that integrates next-generation sequencing, molecular biology techniques, cellular imaging methods, and in vivo animal models. By leveraging these advanced tools and methodologies, we aim to decipher the intricate processes that safeguard the integrity of the genome when replication encounters challenges. This comprehensive understanding not only contributes to our fundamental knowledge of DNA replication and genome maintenance but also lays the foundation for the development of innovative therapeutic strategies to combat cancer.