Liposarcoma is a cancer that affects approximately 1000 new people per year in the United States and primarily targets adults over the age of 50. Although some cases are successfully cured with surgery if caught early, patients traditionally had few options if the cancer came back or if surgery did not eradicate it, because standard chemotherapy and radiation therapy were not effective. A new class of drugs called CDK4/6 inhibitors has recently begun to change the prospects of these patients. These drugs stop cancer cells from dividing without killing them. In some patients, the same drugs cause the cells to enter what is called senescence: the cells never resume dividing, even when the drug is removed. Senescence normally occurs in cells whose DNA has been damaged, so this exciting new form of senescence called SAGA (senescence after growth arrest), that is triggered by a CDK4/6 inhibitor, is not as well understood. I am working with a collaborator who has begun to study SAGA in liposarcoma tumor cells. I am an expert in mapping how DNA is folded inside the cell nucleus to regulate which genes are expressed (turned on). I propose to use my mapping tools to study how the structure of the genome in tumor cells helps cells to decide whether to enter or stay in SAGA, what genes to turn on, and how we might control these genes using other drugs that can be combined with CDK4/6 inhibitors.