Nika Danial

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Associate Professor of Cancer Biology (DFCI)
Associate Professor of Medicine (HMS)
Affiliate member of Cell Biology
Address: 

Longwood Center, Rm 6313

360 Longwood Avenue

Boston, MA 02115

Tel: 
(617) 632-6436
Fax: 
(617) 632-5363
Email: 
Assistant: 
Jollanda Lako
Assistant's Email: 
Assistant's Tel: 
617-582-7176

Nika Danial, Ph.D., is an Associate Professor of Cancer Biology (DFCI) and Medicine (HMS), and an affiliate member of the Cell Biology Department. She received an undergraduate degree in Biological Sciences from Stanford University, and a Ph.D. in Molecular, Cellular and Biophysical Studies from Columbia University. Her postdoctoral studies in the laboratory of Stanley J. Korsmeyer at the Dana-Farber Cancer Institute focused on the role of BCL-2 family proteins in mitochondrial apoptosis, where she discovered a molecular link between cell survival/death regulatory pathways and metabolism. She joined the faculty of the Dana-Farber Cancer Institute and Harvard Medical School in 2005.

The Danial Labfocuses on molecular mechanisms and biologic consequences of cellular fuel choices. Different cell states have distinct anabolic and catabolic needs that are fulfilled by processing specific metabolic substrates. As such, cells’ fuel choice can influence transitions in and out of quiescence, resistance/sensitivity to oxidative stress, metabolic adaptations to nutrient changes, and cell identity, including epigenetic regulation. Understanding how these fuel preferences are controlled and defining their specific metabolic outputs will provide a molecular handle on modulating cell behavior in normal physiology and in pathologic conditions. The Danial lab uses multi-disciplinary in vitroand in vivoapproaches that draw on mitochondrial metabolism, biochemistry, chemical biology, proteomics, metabolomics and genetically engineered mouse models to identify molecular determinants of cellular fuel choices and their effects on cell fate and function. This research program has led to discoveries linking fuel utilization pathways to cellular stress outcomes in diseases such as cancer, diabetes and seizure disorders.