Brian S. Cummings, Ph.D.
Pharmaceutical and Biomedical Sciences
|B.S. Biochemistry/Toxicology||Eastern Michigan University||Ypsilanti||1994|
|Ph.D. Pharmacology||Wayne State University||Detroit||1999|
- Post-doctoral Experience
- Postdoctoral Associate, Univ. Arkansas Medical Sciences, Little Rock, AR, 1999-2001
Postdoctoral Associate, Medical Univ. South Carolina, Charleston, SC, 2001-2003
- Honors and Awards
- Lilly Teaching Fellowship at the University of Georgia, May 2005.
Wayne State University Department of Pharmacology Distinguished Alumni Award
University of Georgia Foreign Travel Assistance Award, August 2004.
Georgia Cancer Coalition, Distinguished Cancer Scientists Award (9/1/03 to
National Institutes of Health National Research Service Award (5/01/00 to
National Institute of Health National Research Service Award, 2000-2003.
1st place Postdoctoral Division 2001 Research Week at the Univ. of Arkansas for Medical Sciences Little Rock, Arkansas, for “Oxidant-Induced Oncosis and Lipid Peroxidation are Increased by Inhibition of Microsomal Ca2+- Independent Phospholipase A2 in Renal Cells,” 2001.
1st place Postdoctoral Division In Vitro Specialty Section 40th Annual Meeting of the Society of Toxicology in San Francisco CA (2001) for “Oxidant-Induced Oncosis and Lipid Peroxidation are Increased by Inhibition of a Microsomal Ca2+-Independent Phospholipase A2 in Renal Cells,” 2001.
- Research Interests
- Primary research interests center on the identification of novel inhibitors of Ca2+-independent phospholipase A2 (iPLA2) as drug therapies for the inhibition of cancer cell growth. My laboratory previously demonstrated that chemical inhibitors of these enzymes altered chemotherapeutic-induced cell death in both kidney and cancer tissues (1,2). Further, we also demonstrated that these enzymes are critical to maintenance of the physicochemical properties of cells by controlling the synthesis of membrane phospholipids (1,3). Current work expanded these finding to cells isolated from human lung, prostate, breast, brain and kidney cancers. Towards this end we have isolated racemic isomers of a previously identified iPLA2 inhibitor called bromoenol lactone (BEL) and demonstrated that R-BEL inhibits the microsomal form of iPLA2 (iPLA2ϐ), while the S-isomers inhibits the cytosolic iPLA2 (iPLA2ϐ) (4). We demonstrated that presence of both of these enzymes in numerous human cancer cell models and demonstrates that S-BEL inhibits cancer cell growth. Thus, S-BEL may represent a novel drug that can be used in combinatorial treatments to increase the effectiveness of classical chemotherapeutics such as cisplatin and vincristine. Other interests in our laboratory include the use of iPLA2 inhibitors as modulators of oxidant-induced injury in neural tissue (5).
- Representative Publications
- B. Sun, X. Zhang, S. Talathi, and B.S. Cummings, Inhibition of Ca2+-independent phospholipase A2 decreases prostate cancer cell growth by p53-dependent and -independent mechanisms. J Pharmacol Exp Ther, 326(1):59-68, 2008.
B. Peterson, Kyndra Stovall, Prashant Monian, James L Franklin and B.S. Cummings, Alterations in phospholipid and fatty acid lipid profiles in primary neocortical cells during oxidant-induced cell injury. Chem Biol Interact, 174(3):163-76, 2008.
S. Jain, X. Zhang, P.J. Khandelwal, A.J. Saunders, B.S. Cummings and P. Oelkers. Characterization of human lysophospholipid acyltransferase 3 (LPCAT3). J Lipid Res, 50(8): 1563-70, 2009.
X. Zhang, D. De Silva, B. Sun, J. Fisher, R.B. Bull, J.A. Cotruvo and B.S. Cummings, Cellular and molecular mechanism of bromate-induced ctotoxicity in human and rat kidney cells, Toxicology, 269(1):13-23, 2010.
B. Sun, X. Zhang, C. Yonz and B.S. Cummings, Inhibition of calcium-independent phospholipase A2 activates p38 MAPK signaling pathways during cytostasis in prostate cancer cells. Biochem Pharmacol, 79(12): 1727-35, 2010.