Dr David Pryce
Lecturer in Biomedical Sciences (Immunology)
School of Medical Sciences
Lab +44 (0)1248 382542
- Molecular Genetics PhD
- Biomolecular Sciences (1st Hons) BSc
I have always had an interest in science, particulariy the life sciences and especially the fascinating world of immunology and the human immune system.
At the age of 18 I obtained a place at Unviersity College London, studying Genetics and Microbiology. Unfortunately, I was unable to complete my studies at UCL, having to return home, to help run the family busines. At the age of 33, I was once again able to return to science, undertaking a BSc Hons degree in Biomolecular Sciences, at Bangor. I have been at Bangor ever since. I completed my PhD in molecular genetics, followed by two externally funded postdoctoral research fellow positions. Finally, in 2010, I acheived a permenant Lecturer position at Bangor, in Biomedical Sciences (immunology).
My research and research led teaching focuses on human molecular immunology and molecular genetics specialising on the roles of the human immune system in autoimmune disease and cancer. I am the organiser and primary deliverer of a number of Undergradute and postgraduate modules, and superviser of research projects associated with the School of Medical Sciences PhD, MRes, MSc and Masters degree programs.
Teaching and Scholarship Roles
- Director of Postgraduate Taught Studies (SMS)
- Director of Internationalisation (SMS)
- Degree 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-2023 International Experience
- MSE-2024 International Experience
- 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 PG Biomedical Sciences, University of Westminster (2012-2016)
- External reviewer for Commision for Academic Accreditation, United Arab Emirates
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.
- Recombination at DNA replication fork barriers is not universal and is differentially regulated by Swi1Pryce, DW, Ramayah, S, Jaendling, A & Mcfarlane, R 2009, 'Recombination at DNA replication fork barriers is not universal and is differentially regulated by Swi1', Proceedings of the National Academy of Sciences of the USA, vol. 106, no. 12, pp. 4770-4775. https://doi.org/10.1073/pnas.0807739106
- The Meiotic Recombination Hotspots of Schizosaccharomyces pombe
- Functional characterisation of the Schizosaccharomyces pombe homologue of the leukaemia-associated translocation breakpoint binding protein translin and its binding partner, TRAX.Mcfarlane, RJ, Jaendling, A, Ramayah, S, Pryce, DW & McFarlane, RJ 2008, 'Functional characterisation of the Schizosaccharomyces pombe homologue of the leukaemia-associated translocation breakpoint binding protein translin and its binding partner, TRAX.', Biochimica et Biophysica Acta - Molecular Cell Research, vol. 1783, no. 2, pp. 203-213. https://doi.org/10.1016/j.bbamcr.2007.10.014
- Linear element-independent meiotic recombination in Schizosaccharomyces pombe.Mcfarlane, RJ, Wells, JL, Pryce, DW, Estreicher, A, Loidl, J & McFarlane, RJ 2006, 'Linear element-independent meiotic recombination in Schizosaccharomyces pombe.', Genetics, vol. 174, no. 3, pp. 1105-1114. https://doi.org/10.1534/genetics.106.063818
- Homologous chromosome pairing in Schizosaccharomyces pombeMcfarlane, RJ, Wells, JL, Pryce, DW & McFarlane, RJ 2006, 'Homologous chromosome pairing in Schizosaccharomyces pombe', Yeast, vol. 23, no. 13, pp. 977-989. https://doi.org/10.1002/yea.1403
- Psc3 cohesion of Schizosaccharomyces pombe: cell cycle analysis and identification of three distinct isoformsIlyushik, E, Pryce, D, Walerych, D, Riddell, T, Wakeman, JA, McInerny, CJ & Mcfarlane, R 2005, 'Psc3 cohesion of Schizosaccharomyces pombe: cell cycle analysis and identification of three distinct isoforms', Biological Chemistry, vol. 386, no. 7, pp. 613-621. https://doi.org/10.1515/BC.2005.072, https://doi.org/10.1515/BC.2005.072
- Differential activation of M26-containing meiotic recombination hot spots in Schizosaccharomyces pombe.Mcfarlane, RJ, Pryce, DW, Lorenz, A, Smirnova, JB, Loidl, J & McFarlane, RJ 2005, 'Differential activation of M26-containing meiotic recombination hot spots in Schizosaccharomyces pombe.', Genetics, vol. 170, no. 1, pp. 95-106. https://doi.org/10.1534/genetics.104.036301
- S-pombe meiotic linear elements contain proteins related to synaptonemal complex componentsLorenz, A, Wells, JL, Pryce, D, Novatchkova, M, Eisenhaber, F, Mcfarlane, RJ & Loidl, J 2004, 'S-pombe meiotic linear elements contain proteins related to synaptonemal complex components', Journal of Cell Science, vol. 117, no. 15, pp. 3343-3351. https://doi.org/10.1242/jcs.01203, https://doi.org/10.1242/jcs.01203
- Royal Society - Equipment Grant: Infra Red Scanning System
Current Research Projects
MRes: Characterisation of the potential of the Ro60 autoimmune antigen as a target for anti-cancer immunotherapy (KESS II funded project BUK2175)
MRes: Characterisation of the potential of the Ro60 autoimmune antigen as a cancer Biomarker (KESS II funded project BUK2178)
MRes: Characterisation of Ro60 splice variants, for potential in targeted treatment of Chronic Myeloid Leukaemia
MRes: Design, validation and utilisation of RT-PCR and qPCR assays for characterisation and quantification of Ro60 autoantigen splice variants in human tissues
MBiol masters: Investigation of the use of anti-sense RNA technologies for specific regulation of expression of the human Ro60 auto-antigen
MSc: Development of targeted Antisense Oligonucleotide agents for enhanced treatment of Chronic Myeloid Leukaemia
MSc: Cloning of human Angiogenin and characterisaion of potential roles of in chronic myeloid leukamia
MSc: Characterisation of ADAR directed, site-specific RNA editing, in leukaemia cell lines
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 stratergies, in which time patients may experience severe side effects and co-morbities, 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 ulimate goal of finding a 'permanant cure' for CML.