Steve Elledge

Steve is widely cited for his many seminal contributions and in particular for his work on the mechanics of both cellular proliferation and the DNA Damage Response. He was awarded the Albert Lasker Prize in Basic Medicine in 2015 for his body of work elucidating how cells sense DNA damage and initiate self-repair. His pioneering research in that field has had a significant impact on understanding human birth defects and aging as well as the genomics of cancer and shows great promise for finding cures. He is also a leader in promoting new genetic technologies and designing methodologies to help researchers better analyze the development of various disorders including cancer, autoimmune diseases and neurodegenerative conditions.

The recipient of numerous other awards including the 2013 Gairdner Foundation international Award, the 2015 Wiley Prize, and the 2017 Gruber Prize in Genetics and the 2017 Breakthrough Prize for Life Sciences for paradigm-shifting research. Dr. Elledge was also a Helen Hay Whitney Fellow, an American Cancer Society Senior Fellow and a Pew Scholar.

Dr. Elledge received his Ph.D. in Biology from the Massachusetts Institute of Technology and his B.S. from the University of Illinois. He completed his post-doctoral studies in the Department of Biochemistry at Stanford University and then joined the faculty of the Baylor College of Medicine in the Department of Biochemistry in 1989 prior to joining Harvard Medical School in 2003.

Elledge’s team is also developing new immunological tools to probe autoimmunity and viral function. One technology they created, called VirScan, detects antibodies against all human viruses in blood. Using a single drop of blood, the method enables researchers to test for current and past viral infections. Others such as T Scan identify the targets of T cells

Elledge’s team recently identified multiple genes that control cell proliferation. The scientists are using this information to reconstruct the higher-order regulatory networks that drive the cell cycle and cancer proliferation. The group has also uncovered many new tumor suppressors and oncogenes by examining the mutational profiles of tumors. They discovered that the distribution of these genes on chromosomes is predictive of the pattern of aneuploidy seen in cancers, providing a new hypothesis of how aneuploidy drives tumorigenesis.