Michael Curran, Ph.D.


November 3, 2016


Dr. Curran joined The University of Texas MD Anderson Cancer Center in 2012 as assistant professor of Immunology. In 2014, he was named scientific director of the Oncology Research for Biologics and Immunotherapy Translation (ORBIT) platform, which coordinates development and production of clinical immunotherapeutic antibodies based on novel targets and preclinical reagents originating at MD Anderson.

Dr. Curran completed B.A. degrees in biology and foreign affairs and a minor in computer science at the University of Virginia in 1995, while receiving accolades for the best undergraduate laboratory research project. He went on to receive a Ph.D. in immunology from Stanford University in 2001, where he was awarded the McDevitt prize for the best graduate thesis in his year. Dr. Curran was the first recipient of the prestigious American Cancer Society Levy Fellowship to fund his postdoctoral studies in the lab of James P. Allison, Ph.D.

While pursuing his postdoctoral studies at Memorial Sloan-Kettering Cancer Center, Dr. Curran published several influential papers describing how T-cell co-stimulatory pathways could be modulated in tandem to mediate immunologic rejection of melanomas in mice. He detailed how combination blockade of the T-cell co-inhibitory receptors CTLA-4 and PD-1 promoted the rejection of a majority of murine melanomas. This work supported the launch of a series of clinical trials in which more than 50 percent of metastatic melanoma patients experienced clinical responses and more than 90 percent survived beyond two years — an unprecedented result that prompted the Food and Drug Administration to make this the first approved immunotherapy antibody combination. In addition, his subsequent immunologic studies of 4-1BB agonist antibodies earned him the Society for the Immunotherapy of Cancer’s prestigious Presidential Award.

In addition to his work on ORBIT, Dr. Curran has established an independent lab at MD Anderson, where his group studies the origins of the immunosuppressive tumor microenvironment and how it can be disrupted to facilitate immune-mediated tumor rejection.