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Brian S. Cummings, Ph.D.
Assistant Professor
Pharmaceutical and Biomedical Sciences
Office: Room 371, R.C. Wilson Pharmacy
Phone: (706) 542-3792
E-mail: bsc@rx.uga.edu
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Biosketch
| B.S. (Biochemistry/Toxicology) | Eastern Michigan University | Ypsilanti, MI | 1994 | | Ph.D. (Pharmacology) | Wayne State University | Detroit, MI | 1999 | | Postdoctoral Associate | Univ. Arkansas Medical Sciences | Little Rock, AR | 1999-2001 | | Postdoctoral Associate | Medical Univ. South Carolina | Charleston, SC | 2001-2003 | | Assistant Professor | University of Georgia | Athens, GA | 2003-present |
Honors and Awards
Lilly Teaching Fellow (2005)
Georgia Cancer Coalition Distinguished Scholar (2003)
2000-2003 National Institute of Health National Research Service Award (Postdoctoral)
Research Interests
My general research interest is in the field of lipid signaling, cell growth and death. Currently, I am studying the role of a Ca2+-independent phospholipase A2 in chemotherapeutic-and oxidant-induced cell death in both cancer cells and in neuronal cell death models. Both of these projects involve lipidomic approaches to understand how phospholipids and fatty acids mediate the above processes. As such, several studies in my laboratory utilize electrospray ionization-mass spectrometry to identify specific phospholipids and fatty acids.
There are two main projects in my laboratory.
Project 1
Project 1 focuses on the role of Ca2+-independent phospholipase A2 in cancer cell growth and death. We recently reported that siRNA inhibition of the cytosolic isoform of Ca2+-independent phospholipase A2 decreased cell growth in correlation with decreases in arachidonic acid-containing phospholipids (Figure 1). These studies suggest that Ca2+-independent phospholipase A2 may be targets for chemotherapeutic intervention of cancer cell growth. These studies also suggest that arachidonic acid-containing phospholipid are critical mediators of cell growth. We have extended these findings to prostate, lung, kidney, brain and leukemia cancer cell models.
Project 2
This project focuses on the role of Ca2+-independent phospholipase A2 in oxidant-induced neuronal cell death. Inhibition of Ca2+-independent phospholipase A2 alters both H202 and tert-butylhydroperoxide (TBHP)-induced cell death in primary cultures of mouse neocoritical cells. Analysis of cellular functions suggest that Ca2+-independent phospholipase A2 function downstream of the initial formation of ROS and lipid peroxidation, but upstream of ATP decreases
(Figure 2). Lipidomic analysis of cells using electrospray ionization mass spectrometry demonstrated that oxidant treatment significantly increased arachidonic acid release. Collectively, these data demonstrate that Ca2+-independent phospholipase A2 mediate oxidant-induced neuronal cell death via a mechanism involving he generation of arachidonic acid.
Representative Publications
Peterson B, Knotts T, Cummings BS. Involvement of Ca2+-independent phospholipase A2 isoforms in oxidant-induced neural cell death. NeuroToxicology, 2007, 28(1):150-60.
Peterson BL, Cummings BS. A review of chromatographic methods for the assessment of phospholipids in biological samples. Biomed. Chromatogr. 2006, 20, 227-43.
Saavedra G, Zhang W, Peterson B, Cummings BS. Differential Roles for Cytosolic and Microsomal Ca2+-Independent Phospholipase A2 in Cell Growth and Maintenance of Phospholipids. J. Pharmacol. Exp. Ther. 2006, 318, 1211-9.
Zhang L, Peterson BL, Cummings BS. The effect of inhibition of Ca2+-independent phospholipase A2 on chemotherapeutic-induced death and phospholipid profiles in renal cells. Biochem. Pharmacol. 2005, 70, 1697-706.
B.S. Cummings and R.G. Schnellmann, Cisplatin-Induced Renal Cell Apoptosis is Mediated by p53 Activation of Caspase 3 Independently of Capase 8 or 9, J. Pharmacol. Exp. Ther., 2002, 302, 8-17.
B.S. Cummings and R.G. Schnellmann, Cisplatin-Induced Renal Cell Apoptosis is Mediated by p53 Activation of Caspase 3 Independently of Capase 8 or 9, J. Pharmacol. Exp Ther., 2002, 302, 8-17.
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