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Office: CAP 1.09a (Office) and BMRC Floor 01 (Lab) E-mail: d.macewan@uea.ac.uk Tel: +44 (0) 1603-592005 School Positions: Professor of Pharmaceutical Cell Biology, Director of Enterprise ResearcherID: http://www.researcherid.com/rid/F-7044-2011 |
Cancer Cell Apoptosis - Epigenetic Control
Nrf2 and HO-1 as a Novel Mechanism in Leukaemia and Lymphoma Drug-Resistance
Switching of Tumour Necrosis Factor Receptor Signalling During Stem Cell Development
Click here to read about Dave's fundraising cycle ride for The Big C.
David MacEwan obtained a BSc (Hons) in Pharmacology from the University of Glasgow in 1988 and a PhD from the MRC Brain Metabolism Unit, University of Edinburgh in 1991. He held postdoctoral Fellowships at Syntex Research Inc. & Stanford University, Palo Alto, California, USA (1991-1994) and the Department of Biochemistry, University of Glasgow (1994-1996). He was a Faculty member in Biomedical Sciences, IMS at the University of Aberdeen between 1996 and 2005, before taking up his current position as Chair in Pharmaceutical Cell Biology, within the School of Pharmacy at the University of East Anglia in 2005. David is a member of the Biochemical Society’s Theme Panel V (Signal Transduction) committee, and is currently a Senior Editor of the British Journal of Pharmacology, a member of the Senior Editorial Board of the American Journal of Cancer Research, and a member of the Editorial Advisory Panels of the Biochemical Journal and Biochemical Pharmacology.
His current research interests are in the investigation of the cell signalling mechanisms of tumour necrosis factor (TNF) receptor subtypes TNFR1 and TNFR2 in apoptotic signalling mechanisms in normal and cancerous tissue, especially laukaemias. The regulation of the signalling machinery by chemotherapeutic agents is also researched to better understand drug-resistant phenotypes of these cancers. In particular we analyse the kinase, proteases, lipases and transcription factors signalling pathways employed by these receptor subtypes, with particular emphasis on the role of NF-κB and Nrf2 anti-apoptotic responsiveness.
Selected Publications
The role of Nrf2 and cytoprotection in regulating chemotherapy.
Rushworth, S.A. and MacEwan, D.J.
Cancers 3, 2011, 1605-1621.
DOI: 10.3390/cancers3021605
Silencing FLIPL modifies TNF-induced apoptotic protein expression
Zaitseva L, Rushworth SA, MacEwan DJ.
Cell Cycle (2011) 10, 1067-1072.
DOI: 10.4161/cc.10.7.15247
High basal nuclear Nrf2 in human AML reduces sensitivity towards proteasome inhibitors
Rushworth SA, Bowles KM., MacEwan DJ.
Cancer Res. (2011) 71, 1999-2009.
DOI: 10.1158/0008-5472.CAN-10-3018
FLIP regulation of HO-1 and TNF signalling in human acute myeloid leukemia provides a unique secondary anti-apoptotic mechanism.
Rushworth SA, Zaitseva L, Langa S, Bowles KM, MacEwan DJ.
Oncotarget (2010) 1, 359-366.
NF-kB–Inhibited Acute Myeloid Leukemia Cells Are Rescued from Apoptosis by Heme Oxygenase-1 Induction
Rushworth, S.A., Bowles, K.M., Raninga, P. and MacEwan, D.J.
Cancer Res (2010) 70, 2973–2983
DOI: 10.1158/0008-5472.CAN-09-3407
HO-1 underlies resistance of AML cells to TNF-induced apoptosis.
Rushworth, S.A. and MacEwan, D.J.
Blood (2008) 111, 3793–3801
DOI: 10.1182/blood-2007-07-104042
Elevated NF-kB responses and FLIP levels in leukemic but not normal lymphocytes: reduction by salicylate allows TNF-induced apoptosis.
Rae, C., Langa, S., Tucker, S.J. and MacEwan, D.J.
Proc. Natl. Acad. Sci. U.S.A. (2007) 104, 12790-12795.
DOI: 10.1073/pnas.0701437104
TNFR1-induced NF-kB, but not ERK, p38MAPK or JNK activation, mediates TNF-induced ICAM-1 and VCAM-1 expression on endothelial cells.
Zhou, Z., Connell, M.C. and MacEwan, D.J.
Cell Signal. (2007) 19, 1238-1248.
DOI: 10.1016/j.cellsig.2006.12.013
