Faye A Rogers PhD
Assistant Professor of Therapeutic Radiology
Breast cancer; Drug design; Altered helical structures; Cancer and genomic instability; DNA repair and apoptosis
Overexpression of HER2, which occurs in ~30% of human breast cancers, correlates with enhanced tumor aggressiveness and decreased patient survival. Although Herceptin has significantly improved the treatment of HER2-positive tumors, drug resistance remains an obstacle in a high fraction of patients. The ability to target these cancers using antitumor agents with mechanisms of action that are independent of HER2 cellular growth function, represents a powerful tool to circumvent this form of resistance. Our lab is interested in the design of novel gene-targeted molecules that can be used in the treatment of both HER2-positive and Hercetin-resistant breast cancers.
- Kaushik Tiwari M, Rogers FA. (2013) XPD-dependent activation of apoptosis in response to triplex-induced DNA damage. Nucleic Acids Res. Aug 2. [Epub ahead of print]
- Rogers, F.A., Hu, R.H., Milstone, L.M. (2012) Local delivery of gene-modifying triplex-forming molecules to epidermis. J. Invest. Dermatol.
- Rogers, F.A., Lin, S.S., Hegan, D.C., Krause, D.S., Glazer, P.M. (2012) Targeted gene modification of hematopoietic progenitor cells in mice following systemic administration of a PNA-peptide conjugate. Molecular Therapy 20(1):109-18.
- Lonkar P, Kim KH, Kuan JY, Chin JY, Rogers FA, Knauert MP, Kole R, Nielsen PE, Glazer PM.Targeted correction of a thalassemia-associated beta-globin mutation induced by pseudo-complementary peptide nucleic acids. Nucleic Acids Res. 2009 Jun;37(11):3635-44. Epub 2009 Apr 13.
- Knauert MP, Lloyd JA, Rogers FA, Datta HJ, Bennett ML, Weeks DL, Glazer PM.
Distance and affinity dependence of triplex-induced recombination.
Biochemistry. 2005 Mar 15;44(10):3856-64.