Ke Completed his PhD evealuating key mechanisms that help prostate cancer cells survive under stress conditions. When cancer cells grow rapidly, they experience internal stress from making too many proteins. Ke discovered two genes (MTHFD2 and MOCOS) that cancer cells rely on to manage this stress, and when he blocked these genes in prostate cancer cells, tumour growth slowed significantly. Through extensive analysis, we found that MTHFD2 was involved in and regulated many other pathways to maintain cancer cell survival, while MOCOS helps regulate cellular building blocks and antioxidant responses. Blocking MOCOS disrupted DNA replication and weakened cancer cells' defences against damage. These findings are particularly significant as they suggest new treatment strategies, especially the possibility of combining MOCOS inhibition with other compounds, such as PARP inhibitors.

Ke is now working on understanding how to enhance Radiotherapy for cancer patients inhibiting key players in DNA damage repair.