Faye A. Rogers, PhD
Assistant Professor, Department of Therapeutic Radiology
| faye.rogers@yale.edu Phone: 203.737.3658 Fax: 203.785.6309 Yale University School of Medicine Department of Therapeutic Radiology 15 York St, HRT 213B P.O. Box 208040 New Haven, CT 06520-8040 |
Degrees/Education:
B.S., Department of Chemistry, Andrews University (1992)
Ph.D., Department of Pharmaceutical Sciences, University of Maryland, Baltimore (1998)
Faculty Appointments:
Associate Research Scientist, Department of Therapeutic Radiology (2003–2007)
Assistant Professor, Yale University School of Medicine, Department of Therapeutic Radiology (2008–Present)
Certifications/Honors:
Kingsley Fellowship in Medical Research
Carl Storm Underrepresented Minority Fellowship
NCI Research Supplement to Promote Diversity in Health–Related Research
Lucille B. Markey Charitable Trust Fellowship
UNCF–Merck Graduate Science Research Dissertation Fellowship
American Association for Cancer Research Scholar
Research Interests:
- Altered Helical Structures
- Cancer and Genomic Instability
- DNA Repair and Apoptosis
Naturally occurring DNA sequences capable of forming non–canonical structures such as H–DNA and cruciforms, are abundant in the human genome and represent a source of genetic instability. These structures are thought to play a role in the expression of several disease–linked genes, including the human c–myc gene. We are interested in determining how cells metabolize such structures in order to provide insight into the pathogenesis of a number of human diseases including cancer. In order to model these structures, we have used a variety of sequence–specific DNA binding molecules, including triplex–forming oligonucleotides (TFOs) and peptide nucleic acids (PNAs), where upon binding to duplex DNA result in the formation of an altered helical structure. We have determined that these structures are recognized and repaired by the nucleotide excision repair (NER) pathway, which occupies an important position in the recognition and repair of a wide array of helix distorting DNA lesions. However, experiments also demonstrate that excessive helical distortions can activate pro–apoptotic pathways. We are currently studying the specific repair processes that recognize and repair altered helical structures and how these structures may trigger the switch from repair to apoptosis when DNA damage presumably overwhelms repair capacity. The maintenance of this mechanism may be of central importance for avoiding progression to cancer.
Training:
Postdoctoral Fellowship: Yale University School of Medicine, New Haven, CT
Mentor: Peter Glazer
