Dr. Groudine received his undergraduate degree from the University of Wisconsin in 1970, and his MD and PhD degrees from the University of Pennsylvania in 1975 and 1976. After post-doctoral training at Princeton University (1976), residency in Radiation Oncology at the University of Washington School of Medicine and research fellowship at Fred Hutch (1976 to 1979), he joined the Fred Hutch faculty in 1979.
Dr. Groudine served as Director of the Hutch’s Basic Sciences Division from 1995 to 2004, Deputy Director of Fred Hutch from 1997 to 2016, Executive Vice President from 2005 to 2016, and as acting President and Director of Fred Hutch in 2014 and 2015.
He is also a professor in the Department of Radiation Oncology and Adjunct Professor in the Department of Pathology at the University of Washington School of Medicine and served on the board of directors of the Seattle Cancer Care Alliance from its inception until 2016. He has served on committees involved in the establishment of national cancer policy, including the Board of Scientific Counselors for the Division of Cancer Treatment at the National Cancer Institute.
Dr. Groudine is internationally known for his work on the regulation of gene expression and its role in carcinogenesis. His work includes uncovering fundamental mechanisms that regulate how genes are turned on and off in normal cells and how the misregulation of these mechanisms lead to cancer.
In recognition of Dr. Groudine¹s contributions to the fields of molecular biology and oncology, he has been elected to the National Academy of Sciences, the National Academy of Medicine (formerly known as The Institute of Medicine) and the American Academy of Arts and Sciences, and as a fellow in the American Association for the Advancement of Science.
Research in the Groudine laboratory focuses on the relationships between gene expression, chromatin structure and the organization of the interphase nucleus during hematopoietic differentiation. They have: (1) analyzed the function of cis-acting regulatory elements in the human and mouse beta-globin loci by targeted deletions (accomplished via homologous and site specific recombination); (2) determined the composition of tissue-specific transcription complexes prior to and after differentiation (by mass spectrometry); and (3) determined the binding of such complexes to regulatory elements by chromatin immune-precipitation (ChIP). They have combined these molecular and biochemical studies with fluorescence in situ hybridization (FISH) to visualize the nuclear location of specific DNA sequences and regulatory proteins during differentiation in vivo and in vitro. Their results suggest a multi-step model for gene activation, involving alterations in the nuclear location of the loci and transactivators, the binding of these factors to regulatory elements in the beta-globin loci, and the subsequent high-level transcription of the beta-globin genes. Their work has also revealed that the mammalian interphase nucleus is organized in a non-random, tissue-specific fashion reflecting the genomic organization and transcription state of genes that are co-regulated during differentiation.