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Gina  DeNicola

Gina DeNicola

Gina DeNicola
Assistant Professor

Contact

Office: SRB 23001
Phone: 813/745-8371
Email: Gina.Denicola@moffitt.org

Education

2010 PhD in Cell and Molecular Biology, The University of Pennsylvania

2010-2016 Postdoc: Beth Israel Deaconess Medical Center, Boston MA, and Weill Cornell Medical College, New York, NY

Research

Cells have energetic and anabolic needs for growth and proliferation. Our research is focused on understanding how cells meet these needs and the mechanisms governing the regulation of tumor metabolism in vivo. While cell culture systems are useful for querying the activity of metabolic pathways, many factors in vivo likely play a major role in the regulation of cellular metabolism, including tumor/stroma interactions, contact with the extracellular matrix, local hypoxia and nutrient availability and nutrient intake by the host. My laboratory investigates the influence of both genomic alterations and the microenvironment on cellular metabolism in vivo.

Mutations in KEAP1 and NRF2, which lead to NRF2 hyperactivation, are commonly found in cancers and lead to metabolic deregulation. Despite the identification of the first KEAP1 mutations in 2006, the precise mechanisms by which NRF2 promotes tumorigenesis are unclear owing to the lack of genetically engineered KEAP1 and NRF2 mutant mouse models that recapitulate the human disease. I, and others, have identified that NRF2 activation leads to profound deregulation of cellular metabolism, including the promotion of serine biosynthesis, which is critical for the proliferation of KEAP1 and NRF2 mutant cells. However, the activity of these metabolic pathways in KEAP1/NRF2 mutant lung tumors in vivo is not established. A major research focus of my lab is investigating how NRF2 promotes tumorigenesis, metabolic deregulation, and metabolic dependencies in vivo using genetically engineered mouse model systems.

My laboratory also focuses on how the microenvironment affects metabolic dependencies. Much of our understanding of tumor metabolism comes from cell culture experiments in which other cell types typically found in tumors, such as fibroblasts and immune cells, are absent. However, these cells have the potential to significantly affect tumor metabolism in vivo by both providing and/or competing for metabolites that the tumor cells require. My laboratory is examining how the metabolic interaction between epithelial tumor cells with fibroblasts and immune cells affects the metabolism and growth of these compartments.

Graduate Students

Brianna