Website: http://www.sph.unc.edu/?option=com_profiles&Itemid=1891&profileAction=ProfDetail&pid=714233563
Email: rfry@email.unc.edu
Voice: (919) 843-6864
The lab focuses on understanding how environmental exposures are associated with human disease with a particular focus on genomic and epigenomic perturbations. Using environmental toxicogenomics and systems biology approaches, we aim to identify key molecular pathways that associate environmental exposure with diseases. A current focus in the lab is to study prenatal exposure to various types of metals including arsenic, cadmium, and lead. We aim to understand molecular mechanisms by which such early exposures are associated with long-term health effects in humans. For example, we are examining DNA methylation profiles in humans exposed to metals during the prenatal period. This research will enable the identification of gene and epigenetic biomarkers of metal exposure. The identified genes can serve as targets for study to unravel potential molecular bases for metal-induced disease. Ultimately, we aim to identify mechanisms of metal-induced disease and the basis for inter-individual disease susceptibility.
]]>Website: http://www.med.unc.edu/ent/research/cancer-research-1/d-neil-hayes-md-mph
Email: hayes@med.unc.edu
Voice: (919) 966-3786
Molecular carcinogenesis, research translation, biomarkers, computational toxicology
]]>Website: http://www.med.unc.edu/kaufmannlab
Email: william.kaufmann@pathology.unc.edu
Voice: (919) 966-8209
Research in the Kaufmann laboratory is concerned with determining the mechanisms whereby cell cycle checkpoints suppress human cancer development. We are focused on two checkpoints that help to stabilize the genome. The decatenation G2 checkpoint delays mitosis until daughter chromatids are sufficiently disentangled by topoisomerase II. This checkpoint is regulated by the breast cancer susceptibility gene BRCA1. The intra-S checkpoint regulates DNA synthesis by controlling the rates of replicon initiation and DNA chain elongation. This checkpoint is regulated by two proteins, Timeless and Tipin, that mediate signaling at stalled replication forks. A program project is studying how the Timeless-Tipin replication fork protection complex protects against UV-induced chromosomal damage and sunlight-induced melanoma.
]]>Website: http://cancer.unc.edu/research/faculty/displayMember.asp?ID=244
Email: cperou@med.unc.edu
Voice: (919) 843-5740
Human carcinomas show great diversity in their morphologies, clinical histories and in their responsiveness to therapy. This wide tumor diversity poses the main challenge to the effective treatment of cancer patients. The main focus of the Perou Lab is to characterize the biology diversity of human tumors using microarray analysis, genomics, molecular genetics, and cell biology, and then to mimic these findings in animal models. We ultimately use these animal systems to develop predictive computational models and to test new therapeutics that are specific for each tumor subtype.
]]>Website: http://www.sph.unc.edu/?option=com_profiles&profileAction=ProfDetail&pid=711650675
Email: dpomp@unc.edu
Voice: (919) 966-0013
Dr. Pomp studies the genetic architecture of complex traits, with an emphasis on body weight regulation and obesity. Using polygenic mouse models and high throughput approaches integrating genomics and physiology, he identifies genes that control predisposition to a variety of complex traits including energy intake and energy expenditure (e.g. voluntary exercise). In addition, Dr. Pomp studies how these genes interact with each other, with changing environments such as nutritional interventions, and with other diseases such as cancer.
]]>Website: http://www.sph.unc.edu/?option=com_profiles&profileAction=ProfDetail&pid=702665970
Email: iir@unc.edu
Voice: (919) 843-2596
Our laboratory applies molecular, biochemical, genetic and genomics approaches to understanding the mechanisms of environmental agent-related organ injury and carcinogenesis. Specifically, we are interested in nuclear receptor-mediated pathways in chemical carcinogenesis, oxidative DNA damage and repair, the role that alcohol and diet play in cancer, and the genetic determinants of the susceptibility to toxicant-induced liver injury. Through a combination of in vivo animal studies and experiments that utilize cellular and molecular models, we aim to better understand why certain chemicals cause cancer or organ damage in rodents and whether humans in general, or any susceptible sub-population in particular, are at risk from similar exposures.
]]>Website: http://pharmacy.unc.edu/Directory/tropsha
Email: alex_tropsha@unc.edu
Voice: (919) 966-2955
The major area of our research is Biomolecular Informatics, which implies understanding relationships between molecular structures (organic or macromolecular) and their properties (activity or function). We are interested in building validated and predictive quantitative models that relate molecular structure and its biological function using statistical and machine learning approaches. We exploit these models to make verifiable predictions about putative function of untested molecules.
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