Assistant Professor, Cancer Research Program; Biology Department
Adjunct Faculty, Department of Pharmacology; UNC-Chapel Hill
Email: abaines@nccu.edu
1991-1995 B.S., Biology, Norfolk State University, Norfolk, VA
1995-2001 Ph.D., Pharmacology and Toxicology, University of Arizona, Tucson, AZ
2001-2006 Postdoctoral Fellow, Depts of Pharmacology and Radiation Oncology, UNC-Chapel Hill
Modified from Hruban et al. (2000) Artwork by Jennifer Parsons-Brumbaugh
The overall focus of our cancer biology research program is two-fold.
- Discover novel molecular targets in cancer, especially pancreatic cancer, which can be targeted by potential cancer therapeutics.
- Understand the role of these molecular targets in the development and progression of normal cells transforming into cancer cells of the pancreas.
Pancreatic cancer is the 4th most common cause of cancer deaths in the United States. Due to the aggressive nature of this cancer and the lack of biomarkers for early detection, the incidence and mortality rates for pancreatic cancer are nearly equivalent. The presence of oncogenically mutated K-Ras in 90% of human pancreatic ductal adenocarcinomas (PDAC) strongly suggests a critical role for this genetic mutation in the development of this disease. Current efforts are focused on inhibitors of Ras downstream signaling. Despite intensive effort, disappointingly, to date no anti-Ras therapies have successfully reached the clinic.
A recent study identified upregulation of the Pim-1 serine/threonine kinase in Ras-mediated transformation of human pancreatic ductal epithelial cells. A second study identified upregulation of the related Pim-3 in PDAC cell lines and patient samples. These observations, when considered together with previous studies implicating Pim kinases as oncogene proteins, provide the foundation for our current studies to determine the functional significance of the Pim kinase family in PDAC growth. We hypothesize that inhibition of Pim function will be an effective approach for antagonizing the aberrant growth of pancreatic carcinoma. To test this hypothesis, we will focus on the following two specific aims: 1. Determine the contribution of upregulated Pim kinase genes in K-Ras mediated transformation of pancreatic cancer. 2. Determine what are important downstream targets of Pim kinases in pancreatic cancer. Results from these studies will allow us to critically validate these kinases as novel therapeutic targets for PDAC treatment.
Rybarczyk, B. J., Baines, A.T., McVey, M., Thompson, J.T., and Wilkins, H. "A Case-based Approach Increases Student Learning Outcomes and Comprehension of Cellular Respiration Concepts", Biochemistry and Molecular Biology Education, Vol. 35, No. 3, pp. 181 -186, 2007.
Lim, K.-H., Baines, A.T., Fiordalisi, J.J., Shipitsin, M., Feig, L.A., Cox, A.D., Der, C.J., and Counter, C.M.: Activation of RalA is critical for Ras-induced tumorigenesis of human cells. Cancer Cell 7:533-545, 2005.
Baines, A.T., Lim, K.-H., Shields, J.M., Lambert, J.M., Counter, C.M., Der, C.J., and Cox, A.D.: Use of retrovirus expression of interfering RNA to determine the contribution of activated K-Ras and Ras effector expression in human tumor cell growth. Methods in Enzymology. Vol. 407, pp. 556-74, 2005.
Baines, A., Taylor-Parker, M., Goulet, A.-C., Renaud, C., Gerner, E.W., and Nelson, M.A.: Selenomethionine
inhibits growth and suppresses cyclooxygenase-2 (COX-2) protein expression in human colon cancer cell lines.Cancer Biology and Therapy1(4):370-4, 2002.
American Association for Cancer Research (AACR)
Society of Toxicology (SOT)