Erik A Bey
Affiliation: University of Texas Southwestern Medical Center
- An NQO1- and PARP-1-mediated cell death pathway induced in non-small-cell lung cancer cells by beta-lapachoneErik A Bey
Department of Pharmacology, Laboratory of Molecular Stress Responses, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA
Proc Natl Acad Sci U S A 104:11832-7. 2007..beta-Lapachone killed cells in a tumorselective manner and is indicated for use against NQO1+ NSCLC cancers...
- Susceptibility of cancer cells to beta-lapachone is enhanced by ionizing radiationHeon Joo Park
Radiobiology Laboratory, Department of Therapeutic Radiology, University of Minnesota Medical School, Minneapolis, MN 55455, USA
Int J Radiat Oncol Biol Phys 61:212-9. 2005..To reveal the interaction between beta-lapachone (beta-lap) and ionizing radiation (IR) in causing clonogenic death in cancer cells and to elucidate the potential usefulness of beta-lap treatment in combination with radiotherapy of cancer...
- Efficacy of beta-lapachone in pancreatic cancer treatment: exploiting the novel, therapeutic target NQO1Matthew Ough
Department of Surgery, University of Iowa College of Medicine, Iowa City, Iowa 52242, USA
Cancer Biol Ther 4:95-102. 2005....
- Calcium-dependent modulation of poly(ADP-ribose) polymerase-1 alters cellular metabolism and DNA repairMelissa S Bentle
Department of Pharmacology, Case Western Reserve University, Cleveland, Ohio 44106, USA
J Biol Chem 281:33684-96. 2006..Thus, Ca(2+) appears to be an important co-factor in PARP-1 hyperactivation after ROS-induced DNA damage, which alters cellular metabolism and DNA repair...
- Beta-lapachone-containing PEG-PLA polymer micelles as novel nanotherapeutics against NQO1-overexpressing tumor cellsElvin Blanco
Simmons Comprehensive Cancer Center, University of Texas Southwestern Medical Center at Dallas, Dallas, TX 75390, United States
J Control Release 122:365-74. 2007..In summary, these data demonstrate the potential of beta-lap micelles as an effective therapeutic strategy against NQO1-overexpressing tumor cells...
- Prostate cancer radiosensitization through poly(ADP-Ribose) polymerase-1 hyperactivationYing Dong
Departments of Pharmacology, Radiation Oncology, Pathology, Biostatistics and Clinical Sciences, and Urology, Simmons Comprehensive Cancer Center, University of Texas Southwestern Medical Center, Dallas, TX 75390 8807, USA
Cancer Res 70:8088-96. 2010..Our findings offer a rationale for the clinical utilization of β-lap (Arq 501) as a radiosensitizer in prostate cancers that overexpress NQO1, offering a potentially synergistic targeting strategy to exploit PARP-1 hyperactivation...
- An NQO1 substrate with potent antitumor activity that selectively kills by PARP1-induced programmed necrosisXiumei Huang
Department of Pharmacology, UT Southwestern Medical Center, Dallas, Texas 75390, USA
Cancer Res 72:3038-47. 2012..Our findings offer preclinical proof-of-concept for deoxynyboquinone as a potent chemotherapeutic agent for treatment of a wide spectrum of therapeutically challenging solid tumors, such as pancreatic and lung cancers...
- Nonhomologous end joining is essential for cellular resistance to the novel antitumor agent, beta-lapachoneMelissa S Bentle
Department of Pharmacology, Case Western Reserve University, Cleveland, OH, USA
Cancer Res 67:6936-45. 2007....
- Intratumoral delivery of beta-lapachone via polymer implants for prostate cancer therapyYing Dong
Simmons Comprehensive Cancer Center, University of Texas Southwestern Medical Center, Dallas, Texas 75390, USA
Clin Cancer Res 15:131-9. 2009....
- Modulating endogenous NQO1 levels identifies key regulatory mechanisms of action of β-lapachone for pancreatic cancer therapyLong Shan Li
Department of Pharmacology, Simmons Comprehensive Cancer Center, University of Texas Southwestern Medical Center at Dallas, Texas 75390, USA
Clin Cancer Res 17:275-85. 2011..Although prior work suggested that β-lapachone (β-lap) could be used for the treatment of pancreatic cancers, the lack of knowledge of the compound's mechanism of action prevented optimal use of this agent...
- Mornings with Art, lessons learned: feedback regulation, restriction threshold biology, and redundancy govern molecular stress responsesErik A Bey
Laboratory of Molecular Stress Responses, Department of Pharmacology and Simmons Comprehensive Cancer Center, University of Texas Southwestern Medical Center at Dallas, 5323 Harry Hines Boulevard, Dallas, TX 75390, USA
J Cell Physiol 209:604-10. 2006..We have learned these lessons and now adopted strategies to exploit them for improved therapy. These examples will be discussed and compared to the pioneering findings of researchers in the Pardee laboratory over the years...
- Superparamagnetic iron oxide nanoparticles: amplifying ROS stress to improve anticancer drug efficacyGang Huang
Departments of Pharmacology, Simmons Comprehensive Cancer Center, University of Texas Southwestern Medical Center at Dallas, Dallas, TX 75390 8807, USA
Theranostics 3:116-26. 2013....
- Dual phosphoinositide 3-kinase/mammalian target of rapamycin blockade is an effective radiosensitizing strategy for the treatment of non-small cell lung cancer harboring K-RAS mutationsGeorgia Konstantinidou
Division of Hematology and Oncology, Simmons Comprehensive Cancer Center, and Hamon Center for Therapeutic Oncology Research, Department of Pathology, University of Texas Southwestern Medical Center, Dallas, Texas TX 75390, USA
Cancer Res 69:7644-52. 2009..These findings may have general applicability in cancer therapy, because aberrant activation of PI3K occurs frequently in human cancer...
- In vivo off-resonance saturation magnetic resonance imaging of alphavbeta3-targeted superparamagnetic nanoparticlesChalermchai Khemtong
Department of Pharmacology, Simmons Comprehensive Cancer Center, University of Texas Southwestern Medical Center, Dallas, Texas 35790, USA
Cancer Res 69:1651-8. 2009..This combination of ORS imaging with a tumor vasculature-targeted, ultrasensitive SPPM design offers new opportunities in molecular imaging of cancer...
- New tricks for old drugs: the anticarcinogenic potential of DNA repair inhibitorsMelissa S Bentle
Department of Pharmacology, Case Western Reserve University, Cleveland, OH 44106, USA
J Mol Histol 37:203-18. 2006..In particular, we focus on a novel anti-tumor agent, beta-lapachone, and its potential to block transformation by modulating poly(ADP-ribose) polymerase-1...
- Review of poly (ADP-ribose) polymerase (PARP) mechanisms of action and rationale for targeting in cancer and other diseasesJulio Morales
Simmons Cancer Center, University of Texas Southwestern Medical Center, Dallas, TX 75399
Crit Rev Eukaryot Gene Expr 24:15-28. 2014..The PARP pathway and its inhibition thus offers a number of opportunities for therapeutic intervention in both cancer and other disease states. ..
- Development of beta-lapachone prodrugs for therapy against human cancer cells with elevated NAD(P)H:quinone oxidoreductase 1 levelsKathryn E Reinicke
Laboratory of Molecular Stress Responses, Case Western Reserve University, Cleveland, OH 44106, USA
Clin Cancer Res 11:3055-64. 2005..e., in the acidic local environment of the tumor tissue), should reduce normal tissue toxicity while eliciting tumor-selective cell killing by NQO1 bioactivation...
- Leveraging an NQO1 Bioactivatable Drug for Tumor-Selective Use of Poly(ADP-ribose) Polymerase InhibitorsXiumei Huang
Departments of Pharmacology and Radiation Oncology, Simmons Comprehensive Cancer Center SCCC, UT Southwestern Medical Center UTSW, Dallas, TX 75390, USA
Cancer Cell 30:940-952. 2016..Synergistic antitumor efficacy and prolonged survival were noted in human orthotopic pancreatic and non-small-cell lung xenograft models, expanding use and efficacy of PARP inhibitors for human cancer therapy...