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Pamela L. Rice, PhD

Assistant Professor


 
Assistant Professor

Education

  • PhD: Department of Pharmaceutical Sciences, School of Pharmacy, University of Colorado Denver
  • PhD in Toxicology, May 1998

Honors and Awards

  • 2000 to 2002 - Postdoctoral Research Fellowship, CRFA
  • 2001 - Brigit Leventhal Scholar-In-Training Award, American Association for Cancer Research
  • 2001 - Keystone Symposia Scholarship, American Gastroenterological Association
  • 1995 - Outstanding Presentation Award, Mountain West Society of Toxicology Mountain West Society of Toxicology, Fort Collins, CO
  • 1993 - Inducted to Rho Chi Society, Pharmaceutical Honor Society, University of Colorado School of Pharmacy

Faculty Appointments

  • 1/04 to present - Assistant Professor, Department of Medicine, University of Colorado Denver
  • 5/01 to 12/03 - Instructor, Department of Medicine, University of Colorado Denver
  • 5/98 to 4/01 - Postdoctoral Research Fellow, Department of Medicine, University of Colorado Denver

National Committees/Responsibilities

Research Incentive Committee, Department of Medicine

Research Interests

My current research focuses on the identification of novel molecular targets for the prevention and treatment of cancer. Normal tissue architecture is maintained by a balance between cell division and programmed cell death, or apoptosis. Tumor cells have evolved intricate mechanisms to bypass this normal balance, leading to their survival advantage. Due to activating mutations in growth-related genes and over-expression of cell survival factors, tumor cells are able to proliferate out of control. My laboratory utilizes tissue culture of human colon and lung tumor cells as models for these diseases, as well as biochemical, pharmacological and molecular biological techniques to identify promising targets for anti-cancer therapy. We have identified several biochemical targets that regulate programmed cell death of colon and lung cancer cells, including the ERK1/2 and PKG proteins. Selective modulation of both ERK1/2 and PKG pathways simultaneously leads to greater tumor cell death than treatment with either compound alone. Taking advantage of such combination therapies in animal and clinical studies is predicted to reduce toxicity and increase efficacy of treatment. Such strategies could dramatically reduce the incidence and mortality of cancer.

Representative Publications

  1. Rice PL, and Ahnen DJ. Sulindac independently modulates extracellular signal-regulated kinase 1/2 and cyclic GMP-dependent protein kinase signaling pathways. Molecular Cancer Therapeutics, 5:746-754, 2006. (download PDF)
  2. Pangburn HA, Kraus H, Ahnen DJ, and Rice PL. Sulindac metabolites inhibit epidermal growth factor receptor activation and expression. Journal of Carcinogenesis, 4:16, 2005. (download PDF)
  3. Rice PL, Beard KS, Driggers LJ, and Ahnen DJ. Inhibition of extracellular-signal regulated kinases 1/2 is required for apoptosis of human colon cancer cells in vitro by sulindac metabolites. Cancer Research, 64:8148-8151, 2004. (download PDF)
  4. Rice PL, Kelloff J, Sullivan H, Driggers LJ, Beard KS, Kuwada S, Piazza G, and Ahnen DJ. Sulindac metabolites induce caspase- and proteasome-dependent degradation of -catenin protein in human colon cancer cells. Molecular Cancer Therapeutics, 2:885-892, 2003. (download PDF)
  5. Rice PL, Washington M, Schleman S, Beard KS, Driggers LJ, and Ahnen DJ. Sulindac sulfide inhibits epidermal growth factor-induced phosphorylation of extracellular-regulated kinase 1/2 and Bad in human colon cancer cells. Cancer Research, 63:616-620, 2003. (download PDF)
  6. Mamay CL, Schauer IE, Rice PL, Dwyer-Nield LD, You M, Sclafani RA, and Malkinson AM. Cyclin D1 as a proliferative marker regulating retinoblastoma phosphorylation in mouse lung epithelial cells. Cancer Letters, 168:165-172, 2001. (download PDF)
  7. Rice PL, Goldberg RJ, Ray EC, Driggers LJ, and Ahnen DJ. Inhibition of extracellular signal-regulated kinase 1/2 phosphorylation and induction of apoptosis by sulindac metabolites. Cancer Research, 61:1541-1547, 2001
  8. Koffler L, Rushong S, Park IK, Cesen-Cummings K, Thompson DC, Dwyer-Nield LD, Rice PL, Mamay C, Malkinson AM, and Ruch RJ. Growth inhibition in G1 and altered expression of cyclin D1 and p27kip-1 after forced connexin expression in lung and liver carcinoma cells.  Journal of Cellular Biochemistry, 79:347-354, 2000