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Deborah Flusberg


PhD Candidate, Program in Biological and Biomedical Sciences and Department of Systems Biology, Harvard Medical School
MSc, Weizmann Institute of Science
BA, Harvard College

Related Work Experience

Scientist, Surface Logix Inc., Brighton, MA (2001-2005)


As a graduate student in the Sorger Lab, I am interested in how a single cellular input can lead to multiple, sometimes conflicting outputs. For example, in response to the apoptosis-inducing ligand TRAIL (TNF-Related Apoptosis Inducing Ligand, currently in clinical trials to treat a variety of cancers), cells turn on both death- and survival-inducing pathways. The resulting response is heterogeneous, even in a clonal population of cells: some cells live, while other cells die. I would like to understand how signaling via these different pathways plays out at the single-cell level, leading to a mixed response. This question has clinical relevance, since many cancers exhibit only partial sensitivity to treatment with TRAIL, and the origins of this are not well understood. From a broader perspective, I am also interested in understanding why one signal might evolve to activate conflicting pathways, and how cancer cells might utilize this strategy to adapt and survive.

Previous interests include relating cytoskeletal and tissue architecture to cell behaviors, such as cell proliferation or cell death. I have also worked on developing novel cell-based assays, using microfabrication techniques, to measure cellular responses to a drug.


Flusberg D, Numaguchi Y, Ingber DE. “Cooperative control of Akt phosphorylation, bcl-2 expression, and apoptosis by cytoskeletal microfilaments and microtubules in capillary endothelial cells.” Mol Biol Cell. 2001 Oct;12(10):3087-94.

Zauberman A, Flusberg D, Haupt Y, Barak Y, Oren M. “A functional p53-responsive intronic promoter is contained within the human mdm2 gene.” Nucleic Acids Res. 1995 Jul 25;23(14):2584-92.

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