Damon Runyon News

Pancreatic cancer may soon become the second leading cause of cancer deaths in the nation. While many cancers have mutations that can be targeted with specific drugs, historically no such targets had been recognized in pancreatic cancer. This changed recently with the discovery that approximately one of every four pancreatic cancers has a defect in the machinery that repairs DNA damage. For example, some have been found to have mutations in the BRCA genes as well as other similar genes involved in repairing double-strand breaks in DNA.

Multiple myeloma (MM) is an incurable cancer of blood cells. It evolves from monoclonal gammopathy of undetermined significance (MGUS), a pre-malignant condition affecting 3-5% of individuals older than 50 years. MGUS patients progress to MM at a rate of 1% per year and the mechanisms underlying such transformation are unknown. No genetic driver mutations have been identified in MM to date, thus limiting our therapeutic options. Signaling through the transmembrane receptor Roundabout1 (ROBO1) is important in solid tumors, particularly gastrointestinal cancer.

Dr. Antal [Robert Black Fellow] aims to develop ways to increase the efficacy of pancreatic cancer chemotherapy. The reason for pancreatic cancer drug resistance is the presence of a dense, supportive tissue surrounding the cancer cells. She is using multiple high-throughput approaches to identify and target key genes within this tissue in order to reduce its supportive role. This work will aid in developing therapies to increase the delivery of the chemotherapeutic drugs to the tumor, allowing immune cells to infiltrate the tumor and kill cancer cells.