Research Topics
Genomes and Genes | Andrew ThorburnSummaryAffiliation: Wake Forest University School of Medicine Country: USA Publications
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Publications
Induction of apoptosis by tumor cell-targeted toxinsA Thorburn
Department of Cancer Biology, Wake Forest University School of Medicine, Medical Center Blvd, Winston Salem, North Carolina 27157, USA
Apoptosis 9:19-25. 2004..In this review, we discuss this strategy, describe ways that the toxins activate the apoptosis machinery and discuss future developments in this field...- Death receptor-induced cell killingAndrew Thorburn
Department of Cancer Biology and Comprehensive Cancer Center, Wake Forest University, Medical Center Boulevard, Winston Salem, NC 27157, USA
Cell Signal 16:139-44. 2004..However, recent studies indicate that we must incorporate new information into this model. Some examples that add new layers of complexity will be discussed in this review... - The C-terminal tails of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) and Fas receptors have opposing functions in Fas-associated death domain (FADD) recruitment and can regulate agonist-specific mechanisms of receptor activationLance R Thomas
Department of Cancer Biology and Comprehensive Cancer Center, Wake Forest University School of Medicine, Winston Salem, North Carolina 27157, USA
J Biol Chem 279:52479-86. 2004.... 
Selective inactivation of a Fas-associated death domain protein (FADD)-dependent apoptosis and autophagy pathway in immortal epithelial cellsJacqueline Thorburn
Department of Cancer Biology, Wake Forest University School of Medicine, Winston Salem, NC 27157, USA
Mol Biol Cell 16:1189-99. 2005..These data identify a novel cell death pathway that combines apoptosis and autophagy and that is selectively inactivated at the earliest stages of epithelial cancer development...- Direct binding of Fas-associated death domain (FADD) to the tumor necrosis factor-related apoptosis-inducing ligand receptor DR5 is regulated by the death effector domain of FADDLance R Thomas
Department of Cancer Biology and Comprehensive Cancer Center, Wake Forest University School of Medicine, Medical Center Blvd Winston Salem, North Carolina 27157, USA
J Biol Chem 279:32780-5. 2004..We conclude that in contrast to current models where the death domain of FADD functions independently of the death effector domain, the death effector domain of FADD comes into direct contact with both TRAIL and Fas/CD95 receptors... - Interstitial diphtheria toxin-epidermal growth factor fusion protein therapy produces regressions of subcutaneous human glioblastoma multiforme tumors in athymic nude miceTie Fu Liu
Department of Medicine, Pathology, and Surgery, Wake Forest University School of Medicine, Winston-Salem, North Carolina 27157, USA
Clin Cancer Res 11:329-34. 2005..c. tumor model and warrants further preclinical testing in an i.c. tumor model for eventual treatment of patients with recurrent or refractory EGF receptor-positive glioblastoma multiforme... - Diphtheria toxin fused to variant interleukin-3 provides enhanced binding to the interleukin-3 receptor and more potent leukemia cell cytotoxicityTie Fu Liu
Department of Medicine and Cancer Biology, Wake Forest University School of Medicine, Winston-Salem, NC, USA
Exp Hematol 32:277-81. 2004..One or both of these variant fusion proteins merit further development for therapy of chemotherapy refractory AML... - Apoptosis by leukemia cell-targeted diphtheria toxin occurs via receptor-independent activation of Fas-associated death domain proteinJacqueline Thorburn
Department of Cancer Biology and Comprehensive Cancer Center, Wake Forest University School of Medicine, Medical Center Boulevard, Winston Salem, North Carolina 27157, USA
Clin Cancer Res 9:861-5. 2003.... - Diphtheria toxin-epidermal growth factor fusion protein and Pseudomonas exotoxin-interleukin 13 fusion protein exert synergistic toxicity against human glioblastoma multiforme cellsTie Fu Liu
Department of Cancer Biology, Wake Forest University School of Medicine, Winston-Salem, North Carolina 27157, USA
Bioconjug Chem 14:1107-14. 2003..These results suggest that both fusion proteins may yield antitumor effects in patients with recurrent gliomas and that combination fusion protein intracranial therapy of malignant gliomas may yield an improved therapeutic index... - Caspase- and serine protease-dependent apoptosis by the death domain of FADD in normal epithelial cellsJacqueline Thorburn
Department of Cancer Biology and Comprehensive Cancer Center, Wake Forest University School of Medicine, Winston-Salem, North Carolina 27157, USA
Mol Biol Cell 14:67-77. 2003..This apoptosis pathway is activated in a cell type-specific manner that is defective in cancer cells, suggesting that this pathway may be targeted during cancer development... - Interleukin-1α mediates the antiproliferative effects of 1,25-dihydroxyvitamin D3 in prostate progenitor/stem cellsSophia L Maund
Department of Cancer Biology, Wake Forest University School of Medicine, Winston Salem, NC, USA
Cancer Res 71:5276-86. 2011..These studies establish a system to study the molecular profile of PrP/SC differentiation, proliferation, and senescence, and they point to an important new role for IL-1α in vitamin D(3) signaling in PrP/SCs... - Regulation of Fas-associated death domain interactions by the death effector domain identified by a modified reverse two-hybrid screenLance R Thomas
Department of Cancer Biology, Comprehensive Cancer Center, Wake Forest University School of Medicine, Medical Center Boulevard, Winston Salem, NC 27157, USA
J Biol Chem 277:34343-8. 2002..These data indicate that in contrast to current models, the death effector domain of FADD is involved in interaction with Fas... - Malignant progenitors from patients with CD87+ acute myelogenous leukemia are sensitive to a diphtheria toxin-urokinase fusion proteinArthur E Frankel
Department of Cancer Biology, Wake Forest University School of Medicine, Winston Salem, NC 27157, USA
Exp Hematol 30:1316-23. 2002..The work also suggests that blast proliferation assays yield similar responses to leukemia colony-forming cell colony assays... - N terminus is essential for tropomyosin functions: N-terminal modification disrupts stress fiber organization and abolishes anti-oncogenic effects of tropomyosin-1Shantaram Bharadwaj
Departments of General Surgery and Cancer Biology, Wake Forest University School of Medicine, Winston Salem, North Carolina 27157, USA
J Biol Chem 279:14039-48. 2004..Our studies provide in vivo functional evidence that the N terminus is a critical determinant of TM1 functions, which in turn determines the organization of stress fibers... - Activation of caspase pathways during iron chelator-mediated apoptosisBryan T Greene
Department of Cancer Biology, and the Comprehensive Cancer Center, Wake Forest University School of Medicine, Winston-Salem, North Carolina 27157, USA
J Biol Chem 277:25568-75. 2002..These results suggest that activation of a mitochondrial caspase pathway is an important mechanism by which iron chelators induce cell death... - Nuclear and cytoplasmic shuttling of TRADD induces apoptosis via different mechanismsMichael Morgan
Department of Cancer Biology and Comprehensive Cancer Center, Wake Forest University School of Medicine, Winston Salem, NC 27157, USA
J Cell Biol 157:975-84. 2002..These data indicate that nucleocytoplasmic shuttling of TRADD leads to the activation of distinct apoptosis mechanisms that connect the death receptor apparatus to nuclear events... - Autophagy in cancer: good, bad, or both?Melanie M Hippert
Department of Pharmacology and University of Colorado Cancer Center, University of Colorado at Denver and Health Sciences Center, Aurora, CO 80045, USA
Cancer Res 66:9349-51. 2006..In this article, we discuss recent discoveries regarding autophagy in cancer... - Mediation of the DCC apoptotic signal by DIP13 alphaJiayou Liu
Department of Pathology, Wayne State University, Detroit, Michigan 48201, USA
J Biol Chem 277:26281-5. 2002..Inhibition of endogenous DIP13 alpha expression by small interfering RNA blocks DCC-induced apoptosis. Our data suggest that DIP13 alpha is a mediator of the DCC apoptotic pathway... - Apoptosis and anthracycline cardiotoxicityAndrew Thorburn
Department of Pharmacology, University of Colorado at Denver and Health Sciences Center, Fitzsimons Campus, P.O. Box 6511, Mail Stop 8303, Aurora, CO 80045, USA
Mol Cancer Ther 5:197-9. 2006 - Regulation of the Pro-apoptotic scaffolding protein POSH by AktTraci R Lyons
Department of Pathology, The University of Colorado at Denver and Health Sciences Center, Aurora, CO 80045, USA
J Biol Chem 282:21987-97. 2007..S304D mutant POSH also shows a strongly reduced ability to induce apoptosis. These findings identify a novel mechanism by which Akt promotes cell survival... - Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) pathway signalingAndrew Thorburn
Department of Pharmacology and University of Colorado Comprehensive Cancer Center, University of Colorado at Denver and Health Sciences Center, Aurora, Colorado 80010, USA
J Thorac Oncol 2:461-5. 2007..This review discusses recent findings about TRAIL pathway signaling and relates the signaling mechanisms to issues that need to be considered as we try to manipulate TRAIL signaling to treat cancer... - Tumor-derived mutations in the TRAIL receptor DR5 inhibit TRAIL signaling through the DR4 receptor by competing for ligand bindingLianghua Bin
Department of Pharmacology, University of Colorado at Denver and Health Sciences Center, Aurora, Colorado 80045, USA
J Biol Chem 282:28189-94. 2007..This study provides a molecular basis for the use of specific therapeutic agonists of TRAIL receptors in people whose tumors harbor somatic DR5 mutations... - TRAIL receptor-targeted therapeutics: resistance mechanisms and strategies to avoid themAndrew Thorburn
Department of Pharmacology, University of Colorado Denver, School of Medicine, Aurora, CO 80010, USA
Drug Resist Updat 11:17-24. 2008....