Staff Collaborate Conference Room

Matthew Riese, MD, PhD

Matthew Riese, MD, PhD

Matthew Riese, MD, PhD

Associate Professor, Medicine (Hematology and Oncology) and Microbiology & Immunology; Associate Investigator, Versiti Blood Research Institute

General Interests

TCR signal transduction and application to tumor immunology


PhD, Microbiology, Medical College of Wisconsin, 2002
MD, Medical College of Wisconsin, Medicine, 2004
Internal Medicine Residency, Brigham and Women's Hospital, Harvard Medical School, 2007
Hematology/Oncology Fellowship, University of Pennsylvania, 2010

Research Interests

Matthew Riese, MD, PhD, is an Associate Professor of Medicine, in the Division of Hematology and Oncology, Department of Medicine at the Medical College of Wisconsin. Dr. Riese graduated with MD and PhD degrees from the Medical College of Wisconsin in 2004 and then completed an internship and residency in internal medicine at Brigham and Women’s Hospital at Harvard Medical School in Boston, Massachusetts. He went on to complete a fellowship in hematology/oncology at the University of Pennsylvania in Philadelphia, Pennsylvania. Dr. Riese is board certified in Internal Medicine and Medical Oncology. He has authored numerous manuscripts and maintains an active research lab focused on augmenting immune-based therapies in the treatment of malignancy. Dr. Riese is interested in investigating immune therapies for genitourinary cancers. He specializes in the treatment of genitourinary malignancies at Froedtert Hospital.

In the field of cancer immunotherapies, much attention has been devoted towards studying the optimal combination of inhibitory T cell surface receptors that can be targeted with to boost anti-tumor T cell activity. Research in the Riese lab focuses on the study of intracellular negative regulators of T cells that may serve as useful targets in cancer treatment. Specifically, the lab focuses on diacylglycerol kinase ζ (dgkζ), a protein that metabolizes the second messenger diacylglycerol (DAG), serving as an off switch for DAG-regulated signaling, including activation of Ras and PKCq. We have found that T cells deficient in dgkζ demonstrate enhanced T cell activity and tumor clearance, both in subcutaneous tumor models, and orthotopic models that utilize T cells engineered to express chimeric antigen receptors (CARs). Work on the lab focuses both on understanding the molecular changes that result from manipulation of dgkζ in T cells, and on translating the work to eventually permit study in human patients.