Uncontrolled growth is a hallmark of cancer where standard treatment options are designed to target rapidly dividing cells. However, the long-term effectiveness of cancer drugs can be hindered by resistance to treatment and tumor recurrence. Studies have shown that relapse can be driven by a population of slow-growing or dormant cancer cells that are not destroyed by initial treatment. Our lab will characterize the origin and impact of this slow-growing population on drug resistance using a specialized live-cell sensor of CDK2, a key protein in driving cell division. We will use this tool to determine the root cause of the slow-cycling state, and to determine whether slow-cycling cells have increased stress and drug resistance. If indeed slow-cycling cells are in a fortified drug-resistant state, the sources of cell stress causing slow-cycling that we identify will suggest ways either to eliminate this stress to return cells to a drug-sensitive state, or to deepen this stress for a lethal effect when combined with another cancer therapeutic. In the long term, this work could offer solutions to combat the emergence of drug-resistant tumors in cancer patients.