- PhD, Cleveland Clinic Lerner Research Institute & Cleveland State University, 2001
Ten Most Recent:
Huang X, Motea EA, Moore ZR, Yao J, Dong Y, Chakrabarti G, Kilgore JA, Silvers MA, Patidar PL, Cholka A, Fattah F, Cha Y, Anderson GG, Kusko R, Peyton M, Yan J, Xie XJ, Sarode V, Williams NS, Minna JD, Beg M, Gerber DE, Bey EA, Boothman DA.
Cancer Cell. 2016; 30(6): 940-952.
Depleting tumor-NQO1 potentiates anoikis and inhibits growth of NSCLC.
Madajewski B, Boatman MA, Chakrabarti G, Boothman DA, Bey EA.
Mol Cancer Res. 2016; 14(1): 14-25.
Review of poly (ADP-ribose) polymerase (PARP) mechanisms of action and rationale for targeting in cancer and other diseases.
Morales JC, Li LS, Fattah FJ, Dong Y, Bey EA, Patel M, Gao JM, Boothman DA.
Crit Rev Eukaryot Gene Expr. 2014; 24(1): 15-28.
Tumor-selective, futile redox cycle-induced bystander effects elicited by NQO1 bioactivatable radiosensitizing drugs in triple-negative breast cancers.
Cao L, Li LS, Spruell C, Xiao L, Chakrabarti G, Bey EA, Reinicke KE, Srougi MC, Moore Z, Dong Y, Vo P, Kabbani W, Yang CR, Wang X, Fattah FJ, Morales JC, Motea EA, Bornmann WG, Yordy JS, Boothman DA.
Antioxid Redox Signal. 2014; 21(2): 237-250.
Hemoglobin-based oxygen carrier mitigates transfusion-mediated pancreas cancer progression.
Lo KK, Bey EA, Patra B, Benson DD, Boothman DA, Silliman CC, Barnett CC, Jr.
Ann Surg Oncol. 2013; 20(6): 2073-2077.
Catalase abrogates beta-Lapachone-induced PARP1 hyperactivation-directed programmed necrosis in NQO1-positive breast cancers.
Bey EA, Reinicke KE, Srougi MC, Varnes M, Anderson VE, Pink JJ, Li LS, Patel M, Cao L, Moore Z, Rommel A, Boatman MA, Lewis C, Euhus DM, Bornmann WG, Buchsbaum DJ, Spitz DR, Gao JM, Boothman DA.
Mol Cancer Ther. 2013; 12(10): 2110-2120.
An NQO1 substrate with potent antitumor activity that selectively kills by PARP1-induced programmed necrosis.
Huang X, Dong Y, Bey EA, Kilgore JA, Bair JS, Li LS, Patel M, Parkinson EI, Wang Y, Williams NS, Gao JM, Hergenrother PJ, Boothman DA.
Cancer Res. 2012; 72(12): 3038-3047.
Modulating endogenous NQO1 levels identifies key regulatory mechanisms of action of beta-lapachone for pancreatic cancer therapy.
Li LS, Bey EA, Dong Y, Meng J, Patra B, Yan J, Xie XJ, Brekken RA, Barnett CC, Jr., Bornmann WG, Gao JM, Boothman DA.
Clin Cancer Res. 2011; 17(2): 275-285.
Prostate cancer radiosensitization through poly(ADP-Ribose) polymerase-1 hyperactivation.
Dong Y, Bey EA, Li LS, Kabbani W, Yan J, Xie XJ, Hsieh JT, Gao JM, Boothman DA.
Cancer Res. 2010; 70(20): 8088-8096.
Beta-lapachone micellar nanotherapeutics for non-small cell lung cancer therapy.
Blanco E, Bey EA, Khemtong C, Yang SG, Setti-Guthi J, Chen H, Kessinger CW, Carnevale KA, Bornmann WG, Boothman DA, Gao JM.
Cancer Res. 2010; 70(10): 3896-3904.
- Case Comprehensive Cancer Center (Case Western Reserve University)
- Simmons Comprehensive Cancer Center (The University of Texas South Western Medical Center at Dallas)
- Cleveland Clinic Foundation (Department of Cell Biology)
- Cleveland State University (Cell Regulatory Biology Program)
- Clarion University of Pennsylvania (B.S. Biology)
About Erik A. Bey
Dr. Bey is an Assistant Professor in the School of Pharmacy and a member of the Sara Crile Allen and James Frederick Allen Lung Cancer Program in the WVU Cancer Institute. His interests include developing novel therapeutics for treatment of lung cancer with a focus on genes that regulate oxidative stress.
Sara Crile Allen and James Frederick Allen Lung Cancer Program
Lung cancer is the leading cause of cancer related deaths in the U.S. and throughout the world. Included among the varying reasons for poor prognosis for lung cancer patients are: the fact that early screening methods are not a standard of care, ineffective therapeutic strategies, and our limited knowledge of pathways that control the transition of normal lung epithelial cells to malignant and invasive lung cancer cells. For example, oxidative stress has been implicated in mutagenic transformation of normal lung epithelial cells. However, the role that oxidative stress regulators play in this process is poorly understood.
Nrf2 is a transcription factor that is activated when cells are confronted with oxidative stress. It then promotes the induction of a variety of cytoprotective genes, which are often elevated in lung tumors vs normal lung epithelial cells. Thus, these cytoprotective genes are hypothesized to play pivotal roles in regulating oxidant stress levels in normal lung and lung tumor cells, as well as their respective microenvironments.
We will use both in vitro and in vivo models to delineate the specific roles that Nrf2 activated genes play in the process of normal lung epithelial transformation, malignant lung tumor cell proliferation and metastases. In addition, we will focus on finding the therapeutic advantages of targeting oxidative stress regulators. Finally, we will also investigate chemotherapies that synergize with ionizing radiation for effective treatment of lung cancers.
Grants and Research
- Oxidative stress and carcinogenesis
- EMT and MET
- Quinone therapeutics
- Orthotopic tumor implantation
- In-vivo drug delivery
- American Association for Cancer Research