Suzanne Jacobs, a group leader and research scientist for the Diabetes Research Group in the Program in Medical and Population Genetics at the Broad Institute of MIT and Harvard, works with functional genomics to identify the causal genes and molecular disease mechanisms that underpin type 2 diabetes. Type 2 diabetes affects more than 300 million people worldwide and has been the subject of many large-scale, genome-wide investigations to identify the genetic roots of the disease.
Jacobs’s work employs diverse molecular, cellular, and animal models to determine the mechanism by which genetic factors contribute to disease. The goal is to identify causal genes and variants as well as the cellular pathways and processes that underlie the biological basis of disease, as these could represent important therapeutic targets for those with or at risk for developing type 2 diabetes.
Jacobs received her bachelor’s degree in biological sciences from Northwestern University and earned a Ph.D. in biomedical sciences from the University of California, San Diego. Before joining the Broad Institute in 2010, Jacobs completed her postdoctoral work in the laboratory of Laura Attardi at the Stanford University School of Medicine’s Department of Radiation Oncology, where she studied the cell death pathway induced by the tumor suppressor protein p53.
Contact Suzanne Jacobs via email at firstname.lastname@example.org.Select Publications
SIGMA Type 2 Diabetes Consortium, et al. Sequence variants in SLC16A11 are a common risk factor for type 2 diabetes in Mexico. Nature. 2014; 506(7486): 97-101.
Flannick J, Thorleifsson G, Beer NL, et al. Loss-of-function mutations in SLC30A8 protect against type 2 diabetes. Nature Genetics. 2014; 45(4): 357-363.
SIGMA Type 2 Diabetes Consortium, et al. Association of a low-frequency variant in HNF1A with type 2 diabetes in a Latino population. JAMA. 2014; 311(22): 2305-14.