Dr Elaine Dunlop

Research Associate

Yr Ysgol Meddygaeth

: dunlopea@cardiff.ac.uk
: +44 (0)29 2068 7785
: Adeilad Geneteg Canser, Ysbyty Athrofaol Cymru, Parc y Mynydd Bychan, Caerdydd, CF14 4XN

: Ar gael fel goruchwyliwr ôl-raddedig

'Working towards tailored therapies for inherited diseases and cancer'

My research centres on the inherited conditions, Tuberous Sclerosis Complex (TSC) and Birt-Hogg-Dubé (BHD) syndrome where patients are predisposed to develop cysts and tumours. I aim to understand what is malfunctioning in these cells at a molecular level, with the goal of identifying weaknesses which could be specifically targeted by therapies. As there is crossover between the altered growth pathways observed in these genetic diseases and the pathways which are at fault in sporadic cancer, these future treatments could also be effective for the wider cancer community. Therefore, through a better understanding of disease processes we can work towards stratifying patients based on the genetics of their disease and treating them with appropriately tailored therapies.

2019

Ni Bhaoighill, M. and Dunlop, E. A. 2019. Mechanistic target of rapamycin inhibitors: successes and challenges as cancer therapeutics. Cancer Drug Resistance 2019(2), pp. 1069-1085. (10.20517/cdr.2019.87)

2018

Johnson, C. E.et al. 2018. Loss of tuberous sclerosis complex 2 sensitizes tumors to nelfinavir−bortezomib therapy to intensify endoplasmic reticulum stress-induced cell death. Oncogene 37, pp. 5913-5925. (10.1038/s41388-018-0381-2)
McCann, H.et al. 2018. Energy stress-mediated cytotoxicity in tuberous sclerosis complex 2-deficient cells with nelfinavir and mefloquine treatment. Cancers 10(10), pp. -., article number: 375. (10.3390/cancers10100375)
Yeung, V.et al. 2018. Rab35-dependent extracellular nanovesicles are required for induction of tumour supporting stroma. Nanoscale 10(18), pp. 8547-8559. (10.1039/C8NR02417K)

2017

Carroll, B. and Dunlop, E. A. 2017. The lysosome: a crucial hub for AMPK and mTORC1 signalling. Biochemical Journal 474(9), pp. 1453-1466. (10.1042/BCJ20160780)
Dunlop, E. A.et al. 2017. Targeting protein homeostasis with nelfinavir/salinomycin dual therapy effectively. Oncotarget (10.18632/oncotarget.16232)

2016

Dodd, K. M. and Dunlop, E. A. 2016. Tuberous sclerosis—A model for tumour growth. Seminars in Cell and Developmental Biology 52, pp. 3-11. (10.1016/j.semcdb.2016.01.025)
Carroll, B.et al. 2016. Control of TSC2-Rheb signaling axis by arginine regulates mTORC1 activity. eLife 5, pp. -., article number: e11058. (10.7554/eLife.11058)

2014

Dunlop, E. and Tee, A. 2014. mTOR and autophagy: a dynamic relationship governed by nutrients and energy. Seminars in Cell and Developmental Biology 36, pp. 121-129. (10.1016/j.semcdb.2014.08.006)
Yan, M.et al. 2014. The tumor suppressor folliculin regulates AMPK-dependent metabolic transformation. Journal of Clinical Investigation 124(6), pp. 2640-2650. (10.1172/JCI71749)
Dunlop, E.et al. 2014. FLCN, a novel autophagy component, interacts with GABARAP and is regulated by ULK1 phosphorylation. Autophagy 10(10), pp. 1749-1760. (10.4161/auto.29640)

2013

Zhang, J.et al. 2013. A tuberous sclerosis complex signalling node at the peroxisome regulates mTORC1 and autophagy in response to ROS. Nature Cell Biology 15(10), pp. 1186-1195. (10.1038/ncb2822)

2012

Thomas, L.et al. 2012. Assessment of the potential pathogenicity of missense mutations identified in the GTPase-activating protein (GAP)-related domain of the neurofibromatosis type-1 (NF1) gene. Human Mutation 33(12), pp. 1687-1696. (10.1002/humu.22162)

2011

Dunlop, E. A.et al. 2011. ULK1 inhibits mTORC1 signaling, promotes multisite Raptor phosphorylation and hinders substrate binding. Autophagy 7(7), pp. 737-747. (10.4161/auto.7.7.15491)
Dunlop, E. A.et al. 2011. Determining the pathogenicity of patient-derived TSC2 mutations by functional characterization and clinical evidence. European Journal of Human Genetics 19(7), pp. 789-795. (10.1038/ejhg.2011.38)
Preston, R. S.et al. 2011. Absence of the Birt-Hogg-Dubé gene product is associated with increased hypoxia-inducible factor transcriptional activity and a loss of metabolic flexibility. Oncogene 30(10), pp. 1159-1173. (10.1038/onc.2010.497)

2010

Soliman, G. A.et al. 2010. mTOR Ser-2481 Autophosphorylation Monitors mTORC-specific Catalytic Activity and Clarifies Rapamycin Mechanism of Action. Journal of Biological Chemistry 285(11), pp. 7866-7879. (10.1074/jbc.M109.096222)
Shi, Z.et al. 2010. Erythropoietin-induced activation of the JAK2/STAT5, PI3K/Akt, and Ras/ERK pathways promotes malignant cell behavior in a modified breast cancer cell line. Molecular Cancer Research 8(4), pp. 615-626. (10.1158/1541-7786.MCR-09-0264)

2009

Dunlop, E. A.et al. 2009. Mammalian target of rapamycin complex 1-mediated phosphorylation of eukaryotic initiation factor 4E-binding protein 1 requires multiple protein-protein interactions for substrate recognition. Cellular Signalling 21(7), pp. 1073-1084. (10.1016/j.cellsig.2009.02.024)
Dunlop, E. A. and Tee, A. 2009. Mammalian target of rapamycin complex 1: Signalling inputs, substrates and feedback mechanisms. Cellular Signalling 21(6), pp. 827-835. (10.1016/j.cellsig.2009.01.012)

2007

Dunlop, E. A., Maxwell, A. P. and Lappin, T. R. J. 2007. Impaired downregulation following erythropoietin receptor activation in non-small cell lung carcinoma. Stem Cells 25(2), pp. 380-384. (10.1634/stemcells.2006-0452)

2006

Brown, W. M.et al. 2006. Erythropoietin receptor expression in non-Small cell lung carcinoma: a question of antibody specificity. Stem Cells 25(3), pp. 718-722. (10.1634/stemcells.2006-0687)
Dunlop, E. A.et al. 2006. Induction of signalling in non-erythroid cells by pharmacological levels of erythropoietin. Neurodegenerative Diseases 3(1-2), pp. 94-100. (10.1159/000092099)

Proffiliau allanol