Barbara Stefanska

Assistant Professor

Research Classification

Nutrition and Cancer
Breast Cancer
Hepatic Diseases
Gene Regulation and Expression

Research Interests

Epigenetics, Cancer epigenetics, Nutritional epigenomics

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Research Methodology

QPCR, Pyrosequencing, western blotting
Microarrays, Next-generation sequencing
bioinformatics
Animal models of human carcinogenesis
cell culture

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Epigenetics refers to the molecular events controlling gene expression that are independent of changes in the underlying DNA sequence. These events include DNA methylation, covalent histone modifications, and non-coding RNA-related mechanisms. Epigenetic modifications of DNA, namely DNA methylation, have been shown to contribute to the etiology of chronic diseases with cancer at the forefront. DNA methylation is dynamic and serves as an adaptive mechanism to a wide variety of environmental factors including diet.

My laboratory is focused on addressing the following scientific questions:

1) Do dietary bioactive compounds act through epigenetic mechanisms to prevent cancer and exert beneficial effects in adjuvant therapy?
Our hypothesis is that dietary polyphenols (e.g., resveratrol, pterostilbene, piceatannol, and coffee polyphenols) impact DNA methylation patterns and thereby gene transcription via modulation of expression and activity of epigenetic enzymes such as TETs and DNMTs. Changes in these enzymes, alter the occupancy of specific protein complexes in gene regulatory regions which determines chromatin structure and as a result gene transcription. Through this mode of action, polyphenols reverse cancer-specific patterns of DNA methylation; they lead to the activation of methylation-silenced tumour suppressor genes and concomitant suppression of demethylation-activated oncogenes and prometastatic genes. We are also exploring if epigenetic mechanisms regulated by polyphenols can sensitize cancer cells to traditional anti-cancer therapeutics.

2) Do dietary bioactive compounds reverse epigenetic aberrations underlying initiation of inflammation and inflammation-driven cancer?
Existing evidence suggests that at sites of inflammation the release of reactive oxygen species causes DNA damage that induces re-localization of epigenetic proteins and results in DNA methylation changes of associated genes during tumorigenesis. We hypothesize that bioactive compounds can prevent cancer development by targeting those changes in the DNA methylation patterns.

3) Do changes in epigenetic marks reflect dietary exposure to bioactive compounds?
We hypothesize that exposure to dietary polyphenols may leave stable marks in human body by inducing changes in DNA methylation patterns. Such molecular markers in easily accessible specimens are needed and should reflect long-term exposures. This will deliver quantitative tools for measuring the intake of bioactive food components in clinical and epidemiological studies.

Current Projects:
1) Epigenetic regulation of the NOTCH oncogenic pathway in response to polyphenols from blueberries and grapes (stilbenoids: pterostilbene, piceatannol, resveratrol).

2) Epigenetic mechanisms of polyphenols in prevention of inflammation in a mouse model of colitis and colon cancer.

3) Epigenetic biomarkers of exposure to dietary bioactive compounds.

Please find more information at:
http://epigenetics.wixsite.com/stefanskalab

 
 

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