Dr Paul Reynolds

Dr Paul Reynolds
Lecturer and Director of Postgraduate Studies



I gained my PhD in 1997 from the Department of Pathology, University of Bristol, in Keith Brown’s lab. In 1998, I became a postdoctoral fellow in Dr Daniel Haber’s lab at Harvard Medical School/Massachusetts General Hospital Cancer Center, USA and then in 2003 I moved to the University of California, San Francisco in order to work with Dr Thea Tlsty investigating the epigenetic modulation of primary human mammary epithelial cells. I was appointed to a Lectureship at the University of St. Andrews in June 2007.

Why do some patients respond to therapy and some don’t? There is a growing need to personalise therapeutic treatments because human diseases are somewhat unique to the individual patient. Diagnostic assays detecting specific features (biomarkers) of a disease provide a framework to classify diseases according to their underlying molecular defects. In turn, the patient-specific molecular profile guides the clinician’s choice for therapy. Cancer is a remarkably heterogenous disease and the increasing complexity of molecular changes that occur during tumour evolution highlights the importance of identifying events that drive this process. Renal podocytes are essential for the normal filtration function of our kidneys. With the increasing use of molecularly targeted cancer therapies, the toxic side-effects of targeted agents are increasingly being recognized and the renal safety of these drugs is becoming an important health issue.

The Reynolds lab is interested in identifying those molecular changes which drive disease with particular emphasis on 1) cancer resistance mechanisms to therapeutic drugs and 2) the mechanobiology of kidney podocytes in health and disease. We are employing biochemistry, molecular biology and cell biology approaches to investigate the nature and context of these factors and how they impact upon human health.

School Roles:

  • Director of Postgraduate Studies (DoPG)

  • School Advisor on Biological Safety

  • Deputy Module Controller MD3002

  • Tissue culture room Curator

data source: symbiosis

Research Overview from research@st-andrews

Systems Pathology and Cancer

Why do some patients respond to therapy and some don’t? There is a growing need to personalise therapeutic treatments because human diseases are somewhat unique to the individual patient. Diagnostic assays detecting specific features (biomarkers) of a disease provide a framework to classify diseases according to their underlying molecular defects. In turn, the patient-specific molecular profile guides the clinician’s choice for therapy. Cancer is a remarkably heterogenous disease and the increasing complexity of molecular changes that occur during tumour evolution highlights the importance of identifying events that drive this process. Renal podocytes are essential for the normal filtration function of our kidneys.  With the increasing use of molecularly targeted cancer therapies, the toxic side-effects of targeted agents are increasingly being recognized and the renal safety of these drugs is becoming an important health issue.

The Reynolds lab is interested in identifying those molecular changes which drive disease with particular emphasis on 1) cancer resistance mechanisms to therapeutic drugs and 2) the mechanobiology of kidney podocytes in health and disease. We are employing biochemistry, molecular biology and cell biology approaches to investigate the nature and context of these factors and how they impact upon human health.

 


Recent publications listed in research@st-andrews
23  (of 23 published available) for par10. (source: University of St Andrews PURE)
Please click title of any item for full details

Genome-scale CRISPR/Cas9 screen determines factors modulating sensitivity to ProTide NUC-1031 In Hwa Um, Tsz Huen Chan, Peter Mullen, David James Harrison, Paul Andrew Reynolds
Scientific Reports 2019 vol.9 
Glutaminase inhibition in renal cell carcinoma therapy Paul Andrew Reynolds
Cancer Drug Resistance 2019 vol.2 
Podocyte injury elicits loss and recovery of cellular forces Nils Michael Kronenberg, David James Harrison, Malte Christian Gather, Paul Andrew Reynolds
Science Advances 2018 vol.4 
Crumbs 3b promotes tight junctions in an ezrin-dependent manner in mammalian cells Nicolas Schlecht, Yanhua Wang, Ailsa Watson, Harinder Hundal, Michael Prystowsky, Frank J Gunn-Moore, Paul Andrew Reynolds
Journal of Molecular Cell Biology 2016 vol.8 pp.439-455
Willing to be involved in cancer Frank J Gunn-Moore, Paul Andrew Reynolds
Genes 2016 vol.7 
Fibroblasts in head neck squamous cell carcinoma associated with perineural invasion have high level nuclear Yes-Associated Protein (YAP) expression Yanghua Wang, Adam Gersten, Frank J Gunn-Moore, Paul Andrew Reynolds, Michael Prystowsky
Academic Pathology 2015 vol.2 
Human tissue in systems medicine Peter David Caie, Klaas Schuur, Anca Oniscu, Peter Mullen, Paul Andrew Reynolds, David James Harrison
FEBS Journal 2013 vol.280 pp.5949–5956
KIBRA Exhibits MST-independent Functional Regulation of the Hippo Signaling Pathway in Mammals Nicole Chang, Andrew Sims, Andrew Steele, Vaila Boswell, Susan Barnett, Christopher Ormandy, Dana Faratian, Frank J Gunn-Moore, Paul Andrew Reynolds
Oncogene 2013 vol.32 pp.1821-1830
The Expanding Family of FERM Proteins. Frank J Gunn-Moore, Paul Andrew Reynolds
Biochemical Journal 2013 vol.452  pp.183-193
Willin, an upstream component of the Hippo signaling pathway, orchestrates mammalian peripheral nerve fibroblasts Calum Patrick, JR Higginson, Maciej Antkowiak, Susan Barnett, Michael Prystowsky, Paul Andrew Reynolds, Frank J Gunn-Moore
PLoS One 2013 vol.8 
Cytoplasmic Ezrin and Moesin Correlate with Poor Survival in Head and Neck Squamous Cell Carcinoma NF Schlecht, M Brandwein-Gensler , RV Smith , N Kawachi, D Broughel, J Lin, CE Keller , Paul Andrew Reynolds, Frank J Gunn-Moore, T Harris, G Childs, TY Belbin, MB Prystowsky
Head and Neck Pathology 2012 vol.6 pp.232-43
Hsa-miR-375 Is Differentially Expressed During Breast Lobular Neoplasia And Promotes Loss Of Mammary Acinar Polarity Orsi Giricz, Paul Andrew Reynolds, Andrew Ramnauth, Christina Liu, Tao Wang, Lesley Stead, Geoffrey Childs, Thomas Rohan, Nella Shapiro, Susan Fineberg, Paraic Kenny, Olivier Loudig
Journal of Pathology 2012 vol.226 pp.108-119
Willin/FRMD6 Expression Activates the Hippo Signaling Pathway Kinases in Mammals and Antagonizes Oncogenic YAP Lissa Rocha Herron, Ashesha Sinha, Xiaomeng Zhang, Magdalena Niestrata, Kishan Dholakia, Michael Prystowsky, Kieran Harvey, Paul Andrew Reynolds, Frank J Gunn-Moore
Oncogene 2012 vol.31 pp.238-250
Sustained induction of epithelial to mesenchymal transition activates DNA methylation of genes silenced in basal-like breast cancers N Dumont, MB Wilson, YG Crawford, Paul Andrew Reynolds, M Sigaroudinia, TD Tlsty
Proceedings of the National Academy of Sciences of the United States of America 2008 vol.105 pp.14867-14872
Morphologically Normal-Appearing Mammary Epithelial Cells Obtained from High-Risk Women Exhibit Methylation Silencing of INK4a/ARF. GR Bean, AD Bryson, PD Pilie, V Goldenberg, JC Baker, C Ibarra, DMU Brander, C Paisie, NR Case, M Gauthier, Paul Andrew Reynolds, E Dietz, J Ostrander, V Scott, LG Wilke, L Yee, BF Kimler, CJ Fabian, CM Zalles, G Broadwater, TD Tlsty, VL Seewaldt
Clinical Cancer Research 2007 vol.13 pp.6834-6841
Tumour Suppressor p16INK4A Regulates Polycomb-mediated DNA Hypermethylation in Human Mammary Epithelial Cells Paul Andrew Reynolds, M Sigaroudinia, G Zardo, MB Wilson, G Benton, C Miller, C Hong, J Fridlyand, JF Costello, TD Tlsty
Journal of Biological Chemistry 2006 vol.281 pp.24790-24802
DOCK4, a GTPase Activator, Is Disrupted during Tumourigenesis. V Yajnik, C Paulding, R Sordella, AI McClatchey, M Saito, DCR Wahrer, Paul Andrew Reynolds, DW Bell, R Lake, S van den Heuvel, J Settleman, DA Haber
Cell 2003 vol.112 pp.673-684
Identification of a DNA-binding site and transcriptional target for the EWS-WT1(+KTS) oncoprotein Paul Andrew Reynolds, GA Smolen, RE Palmer, D Sgroi, V Yajnik, WL Gerald, DA Haber
Genes & Development 2003 vol.17 pp.2094-2107
The parathyroid hormone-responsive B1 gene is interrupted by a t(1;7)(q42;p15) breakpoint associated with Wilms' tumour EG Vernon, K Malik, Paul Andrew Reynolds, R Powlesland, AR Dallosso, S Jackson, K Henthorn, ED Green, KW Brown
Oncogene 2003 vol.22 pp.1371-1380
Induction of BAIAP3 by the EWS-WT1 chimeric fusion implicates regulated exocytosis in tumorigenesis R Palmer, S Lee, J Wong, Paul Andrew Reynolds, H Zhang, V Truong, J Oliner, W Gerald, D Haber
Cancer Cell 2002 vol.2 pp.497-505
Induction of the interleukin-2/15 receptor beta-chain by the EWS-WT1 translocation product JC Wong, SB Lee, MD Bell, Paul Andrew Reynolds, E Fiore, I Stamenkovic, V Truong, JD Oliner, WG Gerald, DA Haber
Oncogene 2002 vol.21 pp.2009-2019
Loss of heterozygosity at 7p in Wilms' tumour development R Powlesland, AK Charles, KTA Malik, Paul Andrew Reynolds, S Pires, M Boavida, KW Brown
British Journal of Cancer 2000 vol.82 pp.323-329
Localization of a novel t(1;7) translocation associated with Wilms' tumor predisposition and skeletal abnormalities Paul Andrew Reynolds, R Powlesland, TJ Keen, C Inglehearn, AE Cunningham, ED Green, KW Brown
Genes, Chromosomes and Cancer 1996 vol.17 pp.151-155