Junran Zhang, MD, PhD
DNA double strand breaks (DSBs) are the most dangerous type of DNA lesion, because incorrectly repaired DSB can result in genomic instability, a major driving force in the onset and development of cancer. Cells that are deficient in DNA DSB repair are sensitive to ionizing radiation (IR) and chemotherapeutic drugs that cause DNA DSBs. Therefore, perturbations of DSB repair that promote carcinogenesis by causing genomic instability may also be the Achilles' heel of cancer. Understanding the molecular mechanisms that are involved in DNA DSB responses has become a central topic in cancer biology and radiation biology.
The goal of my research is to identify the molecular mechanisms maintaining genomic stability and to explore novel strategies targeting cancer cells by studying responses to DNA DSB formation.
Three major ongoing research projects in my group:
- Delineate the role of RNF126 in DNA DSB response and its implications in cancer therapy.
- Determine the mechanisms controlling homologous recombination-mediated repair in response to replication stress, especially at Common Fragile Sites (CFSs). CFSs are the genomic regions prone to form breaks during replication stress and are frequent targets of genomic alterations in both tumors and precancerous lesions.
- Identify novel factors sensitizing cancer cells to ionizing radiation and to CHK1 inhibitors using Decode pooled lentiviral shRNA screening libraries.