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Dr David Pryce

Lecturer in Biomedical Sciences (Immunology)

d.w.pryce@bangor.ac.uk

+44 1248 382363

0000-0002-9713-7307

Dr David Pryce

View Dr David Pryce’s profile on the Bangor Research Portal

Overview

My research and research-led teaching focus on human molecular immunology and molecular genetics specialising on the roles of the human immune system in autoimmune disease and cancer. I am the course organiser of the MSc in Medical Molecular Biology with Genetics program, a primary deliverer of a number of undergraduate and postgraduate modules and a supervisor of research projects associated with the School of Medical and health Sciences PhD, MRes, MSc and Masters degree programs.

Additional Contact Information

Brambell Buidling

Room D11

NWCR institute

School of Medical Sciences

Brambell Building

Deiniol Road

Bangor

Gwynedd

LL57 2UW

 
Office +44 (0)1248 382363

Lab +44 (0)1248 382542

email d.w.pryce@bangor.ac.uk

Qualifications

  • PhD: Molecular Genetics
    1999–2004
  • BSc: Biomolecular Sciences (1st Hons)
    1996

Teaching and Supervision

Course Director MSc in Medical Molecular Biology with Genetics

Academic Supervisor/Mentor Post Graduate Certificate in Higher Education (PGCertHE) (SMS)

PhD examiner, Internal and external

 Module organiser and major deliverer

  • MSE-2014 Human Immunology
  • MSE-4027 Research Skills
  • MSE-4040 Human Molecular Genetics   
  • MSE-4042 Laboratory Molecular Research    
  • MSE-4041 Human Immunology & Disease
  • MSE-4025 Dissertation
  • MSE-4089 Molecular Diagnostics

Teaching and Scholarship Awards

  • Bangor University Teaching Fellow (2012)
  • Recognition of contribution to teaching Excellence CELT Award (2016)

External Teaching and Scholarship

  • External examiner, University of Westminster, PG Biomedical Sciences (2012-2016)

  • External reviewer for Commission for Academic Accreditation, United Arab Emirates (current)

Research Interests

Research overview

Utilising a process termed ‘Immunosurveillance’, our immune system plays a siginficiant role in the battle against cancer. Speciaiised immune cells help identify and destroy Cancerous cells, limit their proliferation and inhibit tumour growth.

Unfortunately however, tumours can evolve mechanisms to avoid and ‘escape’ this immune attack, or indeed can even reprogram immune cells to aid tumour survival and expansion.

Excitingly though, cutting edge research into the agents and mechanisms that regulate our immune system has allowed the development of new cancer-immunotherapies, which can enhance and/or reinvigorate our immune system to once again attack cancerous cells and tumours.

Intriguingly, a number of ‘systemic autoimmune diseases’ - conditions where our immune system mistakenly attacks and damages normal, healthy tissue - are linked to either increased or decreased prevalence of certain Cancers. This suggests key drivers of ‘systemic autoimmunity’ may be involved in either suppressing or enhancing the destruction of certain Cancers and that the ability to identify and regulate key 'systemic auto-antigens' could reveal potent weapons in the fight against Cancer.

The research in my group primarily focuses on investigating the roles of autoantigens, in early stage and advanced cancers, with the aim of identifying novel cancer biomarkers and potential targets for targeted anti-Cancer Immunotherapies.

Postgraduate Project Opportunities

Investigation into drug resistance in Chronic Myeloid Leukaemia Investigation into potential roles of Autoimmune antigens in Cancer development, progression and immunotherapy targets.

Publications

2022

  • PublishedTranslin facilitates RNA polymerase II dissociation and suppresses genome instability during RNase H2- and Dicer-deficiency
    Gomez Escobar, N., Alsaiari, A., Alahmadi, H. A. S., Alzahrani, O., Vernon, E., Althagafi, H., Almobadel, N., Pryce, D., Wakeman, J. & Mcfarlane, R., 17 Jun 2022, In: PLOS Genetics. 18, 6, e1010267.
    Research output: Contribution to journal › Article › peer-review

2021

  • PublishedSouth African and UK hospitalisation data: what it tells us about how deadly omicron is
    Pryce, D., 23 Dec 2021, The Conversation.
    Research output: Contribution to specialist publication › Article

2009

  • PublishedRecombination at DNA replication fork barriers is not universal and is differentially regulated by Swi1
    Pryce, D. W., Ramayah, S., Jaendling, A. & Mcfarlane, R., 24 Mar 2009, In: Proceedings of the National Academy of Sciences of the USA. 106, 12, p. 4770-4775
    Research output: Contribution to journal › Article › peer-review
  • PublishedThe Meiotic Recombination Hotspots of Schizosaccharomyces pombe
    Pryce, D. & Mcfarlane, R. J., 1 Jan 2009, In: Meiosis. 5, p. 1-13
    Research output: Contribution to journal › Article › peer-review

2008

  • PublishedFunctional characterisation of the Schizosaccharomyces pombe homologue of the leukaemia-associated translocation breakpoint binding protein translin and its binding partner, TRAX.
    Mcfarlane, R. J., Jaendling, A., Ramayah, S., Pryce, D. W. & McFarlane, R. J., 1 Feb 2008, In: Biochimica et Biophysica Acta - Molecular Cell Research. 1783, 2, p. 203-213
    Research output: Contribution to journal › Article › peer-review

2006

  • PublishedHomologous chromosome pairing in Schizosaccharomyces pombe
    Mcfarlane, R. J., Wells, J. L., Pryce, D. W. & McFarlane, R. J., 15 Oct 2006, In: Yeast. 23, 13, p. 977-989
    Research output: Contribution to journal › Article › peer-review
  • PublishedLinear element-independent meiotic recombination in Schizosaccharomyces pombe.
    Mcfarlane, R. J., Wells, J. L., Pryce, D. W., Estreicher, A., Loidl, J. & McFarlane, R. J., 1 Nov 2006, In: Genetics. 174, 3, p. 1105-1114
    Research output: Contribution to journal › Article › peer-review

2005

  • PublishedDifferential activation of M26-containing meiotic recombination hot spots in Schizosaccharomyces pombe.
    Mcfarlane, R. J., Pryce, D. W., Lorenz, A., Smirnova, J. B., Loidl, J. & McFarlane, R. J., 1 May 2005, In: Genetics. 170, 1, p. 95-106
    Research output: Contribution to journal › Article › peer-review
  • PublishedPsc3 cohesion of Schizosaccharomyces pombe: cell cycle analysis and identification of three distinct isoforms
    Ilyushik, E., Pryce, D., Walerych, D., Riddell, T., Wakeman, J. A., McInerny, C. J. & Mcfarlane, R., Jul 2005, In: Biological Chemistry. 386, 7, p. 613-621
    Research output: Contribution to journal › Article › peer-review

2004

  • PublishedS-pombe meiotic linear elements contain proteins related to synaptonemal complex components
    Lorenz, A., Wells, J. L., Pryce, D., Novatchkova, M., Eisenhaber, F., Mcfarlane, R. J. & Loidl, J., 28 Jun 2004, In: Journal of Cell Science. 117, 15, p. 3343-3351
    Research output: Contribution to journal › Article › peer-review

Projects

  • KESS II MRes with BEE Robotics- BUK2226

    01/01/2021 – 30/06/2022 (Finished)

  • KESS II MRes with Firestar Science and Technology- BUK2204

    01/10/2019 – 31/10/2020 (Finished)

  • Royal Society - Equipment Grant: Infra Red Scanning System

    01/04/2013 – 31/03/2014 (Finished)

    Links:

    • https://royalsociety.org

Other Grants and Projects

Characterisation of Ro60 splice variants, for potential in targeted treatment of Chronic Myeloid Leukaemia 

The development of Imatinib Mesylate-derivatized Antibody Drug Conjugates for enhanced immunotherapy-based treatment of Chronic Myeloid Leukaemia 

Design, validation and utilisation of RT-PCR and qPCR assays for characterisation and quantification of Ro60 autoantigen splice variants in human tissues

Roles of targeted Antisense Oligonucleotide agents for enhanced treatment of leukaemia

Roles of Angiogenin in chronic myeloid leukaemia

Roles of RNA editing and ADAR1 in leukaemia 

MRes (KESS II) Automation of SARS-CoV-2 and viral pathogen molecular detection

Background to Projects

Chronic myeloid leukaemia (CML) is a form of blood cancer. In a 2013 survey of UK cancers, CML cases comprised 8% of all leukaemias and 0.2% of all new cancer cases. Moreover, UK trends in CML cases mirror comparative global trends, with steady annual increases in both disease incidence and prevalence. 

The discovery of the tyrosine kinase inhibitors (TKIs) - highly specific small molecule drugs which inhibit CML progression - has profoundly reduced CML-dependent mortality. However, several issues still remain with the effectiveness of 'pure' TKI-based therapies, mainly; they are rarely curative, they require long term treatment strategies, in which time patients may experience severe side effects and co-morbidities, but treatment withdrawal can lead to disease relapse, and long-term treatment requires a considerable financial commitment.

Research into enhancing current and developing alternative CML therapy options is, therefore, a vital area of research to sustain current long-term CML treatment strategies and to reach the ultimate goal of finding a 'permanent cure' for CML.

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