Seminar Series: Kay Macleod
Kay Macleod, professor in the Ben May Department for Cancer Research at the University of Chicago, will be a speaker for the Purdue Institute for Cancer Research 2025-26 Seminar Series.
Macleod is a graduate of the University of Edinburgh, Scotland (B.Sc. Hons) and obtained her PhD from the Beatson Institute for Cancer Research at the University of Glasgow, Scotland. Following post-doctoral fellowships at the Pasteur Institute, France and at the MIT Center for Cancer Research, Cambridge, MA, Macleod set up her own research laboratory at the University of Chicago in 2002. Macleod is the Associate Director of Basic Sciences (since 2024) at the University of Chicago Comprehensive Cancer Center and was awarded the Hospira Foundation Professorship in Oncology (in 2024) in recognition of her “outstanding scientific and academic accomplishments“.
Title: Mitophagy and Mitochondrial Stress Responses in Cancer
Research in the Macleod Lab is focused on understanding the role of mitophagy in mitochondrial function and cell signaling and how mitophagy can be targeted in cancers. More broadly, Dr. Macleod’s lab explores the significance of mitochondrial dysfunction in cancer etiology and treatment. In her seminar to be presented at Purdue University on February 19th 2026, Dr. Macleod will present novel findings identifying a novel role for the ATF4 transcription factor as a major sensor of mitochondrial stress in cells and as an essential mediator of KRAS-driven tumorigenesis in pancreatic ductal adenocarcinoma (PDAC). PDAC is the deadliest of all cancers in the US, with only ~13% of patients surviving 5 years after diagnosis and most succumbing to their disease in less than one year. With this high mortality rate and its increased incidence, PDAC is set to replace colorectal cancer as the second leading cause of cancer deaths in the US by 2030. Dr. Macleod and colleagues identified a ATF4 gene expression signature that is highly predictive of human PDAC patient outcomes and have now shown that deletion of Atf4 in genetically engineered mouse models of PDAC completely inhibited malignant PDAC. Macleod Lab research determined that loss of ATF4 causes DNA damage in incipient tumor cells leading to p53-dependent cell death thereby preventing development of PDAC. This was due to disrupted one-carbon (1C)-metabolism arising from decreased expression of ATF4 target genes essential for nucleotide biosynthesis. These defects were rescued by a high serine diet while PDAC tumorigenesis was restored by targeted p53 deletion. These findings provide compelling evidence that targeting ATF4 in PDAC could be highly impactful in treating patients in the clinic.
This event is hosted by Brittany Allen-Petersen.