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Application of Human Genomics to Population Sciences: Molecular Prevention

  • Full or part time
  • Application Deadline
    Applications accepted all year round
  • Self-Funded PhD Students Only
    Self-Funded PhD Students Only

About This PhD Project

Project Description

The Environmental Public Health Functional Genomics Group has been engaged in characterizing underlying genetic, epigenetic and environmental factors that contribute to variability in human responses to endocrine disrupting stressors. We especially focus on discovery of human DNA variants and epigenetic, stochastic and environmental factors that modify responses to exposure to endocrine disrupting stressors and how these factors affect the susceptibility to complex chronic diseases, such as cancer, neurodegenerative lesions in exposed people. These information may prove useful in developing therapeutic targets for the molecular prevention and treatment of complex chronic diseases and discovery of valuable novel biomarkers for identifying at-risk individuals and devising chronic human disease-molecular prevention strategies.

Major areas of research:
1. Identifying the biological pathways by which reactive oxygen species (ROS) increase an individual’s susceptibility to develop aggressive antiestrogen-independent metastatic breast cancer via influencing a redox sensitive transcription factor - Nuclear Respiratory Factor-1 (NRF-1).

2. Evaluation of pathoepigenetic/genetic mechanisms of glioblastoma and role of gene-endocrine disruptor interactions in brain health.

3. Integrative stochastic modelling to identify biological pathways and networks contributing to the susceptibility of cancer and neurodegenerative diseases.

4. Developing targeted stem cell nano therapy of cancer and other environmental chronic complex human diseases


References

Luna B, Bhatia S, Yoo C, Felty Q, Sandberg DI, Duchowny M, Khatib Z, Miller I, Ragheb J, Prasanna J, Roy D. Bayesian Network and Mechanistic Hierarchical Structure Modeling of Increased likelihood of Developing Intractable Childhood Epilepsy from the Combined Effect of mtDNA Variants, Oxidative Damage, and Copy Number. J Mol Neurosci. 2014 Jul 16 2.

Okoh V, Felty Q, Parkash J, Poppiti R, Roy D.Reactive oxygen species via redox signaling to PI3K/AKT pathway contribute to the malignant growth of 4-hydroxy estradiol-transformed mammary epithelial cells. PLoS One. 2013;8(2):e54206

Penney RB, Roy D. Thioredoxin-mediated redox regulation of resistance to endocrine therapy in breast cancer. Biochim Biophys Acta. 2013 Aug;1836(1):60-79

Okoh V, Deoraj A, Roy D: Estrogen-induced reactive oxygen species-mediated signalings contribute to breast cancer. Biochim Biophys Acta, 2010, 1815(1):115-133

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