Dr Vignir Helgason

Reader (Translational Research Centre)

telephone: 0141 330 7245
email: Vignir.Helgason@glasgow.ac.uk

Institute of Cancer Sciences, Wolfson Wohl Cancer Research Centre, Garscube Estate, Glasgow, Bearsden, G61 1QH

ORCID iD https://orcid.org/0000-0003-1616-132X

Biography

Dr Vignir Helgason is a Reader in Cancer Research at the Institute of Cancer Sciences, University of Glasgow.

Dr Helgason graduated with a B.Sc. in Biology from the University of Iceland in 2000 and worked at deCODE genetics (Reykjavik, Iceland) for three years before embarking on an academic career. He trained for a PhD degree in Prof. Kevin Ryan’s “Tumour Cell Death Laboratory” at the Cancer Research UK Beatson Institute and graduated with a PhD from University of Glasgow in October 2007.

Dr Helgason held two post-doctoral positions in Prof. Tessa Holyoake’s lab at the Paul O’Gorman Leukaemia Research Centre, which has been described as “a flagship model of integrated basic, translational and clinical research.”

In 2013, Dr Helgason was awarded a Kay Kendall Leukaemia Fund Research Fellowship that supports “truly outstanding biomedical scientists prior to establishing an independent research group in an international centre of excellence”. This facilitated a successful application to the University of Glasgow’s flagship Leadership Fellowship scheme, which allowed Dr Helgason to setup his own research group at the world-class Wolfson Wohl Cancer Research Centre (WWCRC).

Additionally, Dr Helgason was awarded the John Goldman Fellowship for Future Science, a prestigious award aimed at those with “passion for science, a desire to develop new ideas and translate scientific advances into clinical practice”.

Through additional studentship/grant applications, collaborations, conferences, meetings and high-impact publications Dr Helgason achieved a promotion to a Reader in Cancer Research position in August 2020.

Research interests

Leukaemia Stem Cells - Autophagy - Cancer Metabolism - Leukaemia Niche.

Dr Helgason’s team focuses on “Bench to Bedside” translational research and is directly in line with Wolfson Wohl Cancer Research Centre, CRUK Beatson Institute and CRUK Glasgow Cancer Centre vision and strategy. So far, the team has primarily focused on Chronic Myeloid Leukaemia (CML), a tumour type in which Glasgow has particular clinical expertise and excising translational projects.

The team has emerging interest in related leukaemias and myeloproliferative neoplasms, with the overall aim of targeting appropriate therapy to the stem cell compartment to remove the population in which drug resistance occurs. All on-going projects relate to targeting: “Leukaemia Stem Cells” - “Autophagy” - “Cancer Metabolism” - “Leukaemia Niche”.

Publications

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Number of items: 30.

2020

Sepp, K., Lee, M., Bluntzer, M., Helgason, G. V. , Hulme, A. N. and Brunton, V. G. (2020) Utilizing stimulated Raman scattering microscopy to study intracellular distribution of label-free ponatinib in live cells. Journal of Medicinal Chemistry, 63(5), pp. 2028-2034. (doi: 10.1021/acs.jmedchem.9b01546) (PMID:31829628) (PMCID:PMC7073915)

Vetrie, D. , Helgason, V. and Copland, M. (2020) The leukaemia stem cell: similarities, differences and clinical prospects in CML and AML. Nature Reviews Cancer, 20, pp. 158-173. (doi: 10.1038/s41568-019-0230-9) (PMID:31907378)

2019

Baquero, P., Dawson, A. and Helgason, G. V. (2019) Autophagy and mitochondrial metabolism: insights into the role and therapeutic potential in chronic myeloid leukaemia. FEBS Journal, 286(7), pp. 1271-1283. (doi: 10.1111/febs.14659) (PMID:30222247)

Baquero, P. et al. (2019) Targeting quiescent leukemic stem cells using second generation autophagy inhibitors. Leukemia, 33(4), pp. 981-994. (doi: 10.1038/s41375-018-0252-4) (PMID:30185934) (PMCID:PMC6292500)

Smith, L. D. et al. (2019) BCR signaling contributes to autophagy regulation in chronic lymphocytic leukemia. Leukemia, 34, pp. 640-644. (doi: 10.1038/s41375-019-0557-y) (PMID:31462734) (PMCID:PMC6995694)

2018

Ianniciello, A., Rattigan, K. M. and Helgason, G. V. (2018) The ins and outs of autophagy and metabolism in hematopoietic and leukemic stem cells: food for thought. Frontiers in Cell and Developmental Biology, 6, 120. (doi: 10.3389/fcell.2018.00120) (PMID:30320108) (PMCID:PMC6169402)

Mitchell, R. et al. (2018) Targeting BCR-ABL independent TKI resistance in chronic myeloid leukaemia by mTOR and autophagy inhibition. Journal of the National Cancer Institute, 110(5), pp. 467-478. (doi: 10.1093/jnci/djx236) (PMID:29165716) (PMCID:PMC5946859)

Pellicano, F. et al. (2018) Hsa-mir183/EGR1-mediated regulation of E2F1 is required for CML stem/progenitor cell survival. Blood, 131(14), pp. 1532-1544. (doi: 10.1182/blood-2017-05-783845) (PMID:29437554) (PMCID:PMC6027092)

de Beauchamp, L., Baquero, P., Kuntz, E. M., Gottlieb, E. and Helgason, G. V. (2018) Auto-commentary on: “Targeting mitochondrial oxidative phosphorylation eradicates therapy-resistant chronic myeloid leukemia stem cells”. Molecular and Cellular Oncology, 5(1), e1403532. (doi: 10.1080/23723556.2017.1403532) (PMID:28920959) (PMCID:PMC5657469)

2017

Kuntz, E. M., Baquero, P., Michie, A. M. , Dunn, K., Tardito, S. , Holyoake, T. L., Helgason, G. V. and Gottlieb, E. (2017) Targeting mitochondrial oxidative phosphorylation eradicates therapy-resistant chronic myeloid leukemia stem cells. Nature Medicine, 23(10), pp. 1234-1240. (doi: 10.1038/nm.4399) (PMID:28920959) (PMCID:PMC5657469)

Horne, G. , Jackson, L. , Helgason, V. and Holyoake, T. L. (2017) Stem cell guardians – old and new perspectives in LSC biology. Current Drug Targets, 18(4), pp. 405-413. (doi: 10.2174/1389450117666160712092944) (PMID:27411711)

2016

Schemionek, M. et al. (2016) MTSS1 is a critical epigenetically regulated tumor suppressor in CML. Leukemia, 30(4), pp. 823-830. (doi: 10.1038/leu.2015.329) (PMID:26621336)

Karvela, M. et al. (2016) ATG7 regulates energy metabolism, differentiation and survival of Philadelphia chromosome-positive cells. Autophagy, 12(6), pp. 936-948. (doi: 10.1080/15548627.2016.1162359) (PMID:27168493) (PMCID:PMC4922442)

2015

Holyoake, T. L. and Helgason, G. V. (2015) Do we need more drugs for chronic myeloid leukemia? Immunological Reviews, 263(1), pp. 106-123. (doi: 10.1111/imr.12234) (PMID:25510274)

2014

Pellicano, F. et al. (2014) The antiproliferative activity of kinase inhibitors in chronic myeloid leukemia cells is mediated by FOXO transcription factors. Stem Cells, 32(9), pp. 2324-2337. (doi: 10.1002/stem.1748) (PMID:24806995) (PMCID:PMC4282530)

2013

Nencioni, A., Cea, M., Montecucco, F., Longo, V.D., Patrone, F., Carella, A.M., Holyoake, T.L. and Helgason, G.V. (2013) Autophagy in blood cancers: biological role and therapeutic implications. Haematologica, 98(9), pp. 1335-1343. (doi: 10.3324/haematol.2012.079061)

Helgason, G.V. , Mukhopadhyay, A., Karvela, M., Salomoni, P., Calabretta, B. and Holyoake, T.L. (2013) Autophagy in chronic myeloid leukaemia: stem cell survival and implication in therapy. Current Cancer Drug Targets, 13(7), pp. 724-34.

Helgason, G.V. , Holyoake, T.L. and Ryan, K.M. (2013) Role of autophagy in cancer prevention, development and therapy. Essays in Biochemistry, 55(1), pp. 133-151. (doi: 10.1042/BSE0550133)

2012

Klionsky, D. J. et al. (2012) Guidelines for the use and interpretation of assays for monitoring autophagy. Autophagy, 8(4), pp. 445-544. (doi: 10.4161/auto.19496) (PMID:22966490) (PMCID:PMC3404883)

Karvela, M., Mukhopadhyay, A., Allan, E., Helgason, G.V. and Holyoake, T. (2012) Specific inhibition of autophagy enhances TKI-induced death in CML cells. British Journal of Haematology, 157(S1), p. 58. (doi: 10.1111/j.1365-2141.2012.09071.x)

MacKay, C.E., Allen, E.K., Mukhopadhyay, A., Karvela, M., Holyoake, T., Jorgensen, H. and Helgason, V. (2012) Effect of BCR-ABL inhibition on induction of autophagy in chronic myeloid leukaemia cells. British Journal of Haematology, 157(S1), p. 58. (doi: 10.1111/j.1365-2141.2012.09071.x)

Karvela, M., Helgason, G. V. and Holyoake, T. L. (2012) Mechanisms and novel approaches in overriding tyrosine kinase inhibitor resistance in chronic myeloid leukemia. Expert Review of Anticancer Therapy, 12(3), pp. 381-392. (doi: 10.1586/ERA.12.10) (PMID:22369329)

Hamilton, A. et al. (2012) Chronic myeloid leukemia stem cells are not dependent on Bcr-Abl kinase activity for their survival. Blood, 119(6), pp. 1501-1510. (doi: 10.1182/blood-2010-12-326843)

2011

Helgason, G. V. , Karvela, M. and Holyoake, T. L. (2011) Kill one bird with two stones: potential efficacy of BCR-ABL and autophagy inhibition in CML. Blood, 118(8), pp. 2035-2043. (doi: 10.1182/blood-2011-01-330621)

Mukhopadhyay, A., Helgason, G. V. , Karvela, M. and Holyoake, T. L. (2011) Hydroxychloroquine for chronic myeloid leukemia: complete cure on the horizon? Expert Review of Hematology, 4(4), pp. 369-371. (doi: 10.1586/ehm.11.34)

Pellicano, F., Simara, P., Sinclair, A., Helgason, G.V. , Copland, M. , Grant, S. and Holyoake, T.L. (2011) The MEK inhibitor PD184352 enhances BMS-214662-induced apoptosis in CD34+ CML stem/progenitor cells. Leukemia, 25(7), pp. 1159-67. (doi: 10.1038/leu.2011.67)

2010

Helgason, V. , Young, G. and Holyoake, T. (2010) Targeting chronic myeloid leukemia stem cells. Current Hematologic Malignancy Reports, 5(2), pp. 81-87. (doi: 10.1007/s11899-010-0043-0)

Helgason, G.V. , O'Prey, J. and Ryan, K.M. (2010) Oncogene-induced sensitization to chemotherapy-induced death requires induction as well as deregulation of E2F1. Cancer Research, 70(10), pp. 4074-4080. (doi: 10.1158/0008-5472.CAN-09-2876)

2009

Bellodi, C. et al. (2009) Targeting autophagy potentiates tyrosine kinase inhibitor–induced cell death in Philadelphia chromosome–positive cells, including primary CML stem cells. Journal of Clinical Investigation, 119(5), pp. 1109-1123. (doi: 10.1172/JCI35660)

Myssina, S. et al. (2009) Combined BCR-ABL inhibition with lentiviral-delivered shRNA and dasatinib augments induction of apoptosis in Philadelphia-positive cells. Experimental Hematology, 37(2), pp. 206-214. (doi: 10.1016/j.exphem.2008.10.013)

This list was generated on Sun Feb 28 23:42:46 2021 GMT.

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