Dr. Mancias is a Radiation Oncology physician-scientist who runs a laboratory studying critical aspects of pancreatic cancer biology and maintains a clinical practice caring for patients diagnosed with pancreatic cancer. Dr. Mancias graduated from the Tri-Institutional Weill Cornell/Rockefeller/Sloan-Kettering MD-PhD program in 2008. He completed a residency in Radiation Oncology in the Harvard Radiation Oncology Program in 2013. His postdoctoral research at Harvard Medical School and Dana-Farber Cancer Institute focused on the role of autophagy in pancreatic cancer. In 2016, Dr. Mancias began his independent research and clinical program at DFCI / Brigham and Women’s Hospital and as an investigator within the DFCI Hale Family Center for Pancreatic Cancer Research. His research program studies the role of autophagy, iron metabolism, and therapeutic resistance in pancreatic ductal adenocarcinoma (PDAC) using a combination of genetic, quantitative proteomic, cell biological, and mouse modeling approaches. The unique importance of autophagy in PDAC suggests that there may be a subset of proteins that are specifically targeted by autophagy for degradation, which would promote proliferation and survival. Using a quantitative pancreatic cancer autophagosomal proteomics approach, Dr. Mancias identified NCOA4 as the autophagy receptor for ferritin autophagy and degradation (ferritinophagy). Dr. Mancias and his lab further identified that ferritinophagy is a highly regulated process and plays a central role in the larger context of cellular and organismal iron homeostasis. Given the reliance of PDAC on both high levels of autophagy as well as iron, the Mancias Lab subsequently identified that NCOA4-mediated ferritinophagy is a PDAC dependency and therapeutic target critical for maintenance of PDAC iron homeostasis. Furthermore, in collaboration, the Mancias Lab has determined that NCOA4-mediated ferritinophagy is further upregulated in PDAC in response to KRAS/MAPK pathway inhibition thereby nominating KRAS and ferritinophagy inhibition as a promising combination therapy to circumvent resistance to KRAS inhibition.