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Rebecca Fry

Rebecca Fry, PhD, is a UNC Lineberger Comprehensive Cancer Center member and Assistant Professor of Environmental Sciences & Engineering at UNC-Chapel Hill Gillings School of Global Public Health.

Assistant Professor
UNC-Chapel Hill
Cancer Genetics

Area of interest

The Fry lab uses toxicogenomic and systems biology approaches to reveal molecular mechanisms of metal-induced carcinogenesis. A primary focus of our laboratory includes the study of mechanisms of arsenic-induced disease. A broad goal of the laboratory is to identify the genes and their encoded proteins that control human susceptibility to metal-induced disease. Active and proposed studies include:

Determining the role of NF-kB in arsenic-induced disease.
Arsenic exposure in humans is associated with increased risk for many types of cancers, but the mechanism for this is unclear. In addition, arsenic is a known co-carcinogen with DNA damaging agents. We have shown that prenatal arsenic exposure in humans results in significant transcriptional modulation of the NF-kB pathway. We hypothesize that this modulation may impact cellular responses upon exposure to DNA damaging agents. Specifically, we are using a lymphoblastoid cell culture model to determine the impact of low dose arsenic exposure on modulation of the NF-kB pathway. As our research is also aimed at identifying mechanisms by which arsenic acts as a co-carcinogen, we are examining how low dose arsenic exposure impacts responses to subsequent exposure to DNA damaging agents. Our work in vitro is complemented by our studies in human populations where we examine the impact of exposure on NF-kB activation. These studies examine a mechanism by which arsenic exposure could modulate cellular responses to other damaging agents and be linked to cancer.

Identifying proteins that protect against arsenic-induced killing; application of arsenic as a chemotherapeutic. Arsenic trioxide is used as a chemotherapeutic to treat leukemia. In these studies we perform computational analysis that integrates tumor cell responses to arsenic with genome-wide expression profiles. These analyses are used to identify genes that influence tumor cell sensitivity to against arsenic-induced cytotoxicity. Using these approaches, we have identified pathways that are associated with cellular resistance to arsenic. These pathways are being targeted to generate knockdown cells to determine if altered expression impacts tumor cell survival. These studies have direct application in the clinic where arsenic could be used to treat other types of tumors.

Awards and Honors

  • 2005 Infinite Mile Award, MIT
  • 1995 Phi Beta Kappa (William Smith College)
  • 1995 Magna Cum Laude (William Smith College)

Link to Publications on Reach NC site