I am a senior lecturer in the Division of Cancer Sciences within the School of Medical Sciences in the Faculty of Biology, Medicine and Health. Research in my laboratory focuses on the link between metabolism and cytosolic calcium signalling during pancreatitis and pancreatic cancer (see Research Interests). I predominantly teach Pharmacology and Physiology to undergraduate Science and Pharmacy students.

 

I graduated from the University of Manchester with a BSc in Pharmacology and Physiology (1995) and then with a PhD in Physiology (1998). I spent a brief period (1998-1999) as a postdoc in the Department of Medicine here in Manchester working on the effects of hypoxia on vascular tone, prior to a move across the pond to the University of Rochester Medical Center, NY.  Here I worked as a postdoc and later as a Research Assistant Professor, where I developed an interest in signalling cross-talk in secretory epithelia which has formed the basis of some of my current research projects (see Research Interests).

 

I recently spent a research sabbatical working in the Department of Molecular and Integrative Medicine at the University of Michigan in collaboration with Prof John Williams. Here I learnt in vivo techniques and developed new models of pancreatitis combined with the hyperinsulinaemic euglycaemic clamp. This allows the administration of insulin during induction of pancreatitis while maintaining tight control of blood glucose.

My research group is interested in pancreatitis and pancreatic cancer. Both these diseases affect the epithelial cells of the pancreas involved in the secretion of a fluid containing all the enzymes required to digest food in the gut. Pancreatitis is a serious and sometimes fatal inflammatory disease where this process goes wrong and the pancreas digest itself. Growing evidence from research suggests that impairment of metabolism, which generates cellular energy, and the control of cellular calcium, which stimulates secretion, both trigger pancreatitis. This leads to catastrophic cell death causing the digestive enzymes to spill out of the pancreas causing autodigestion. Pancreatic cancer is one of the most aggressive and deadly cancers, where the vast majority of patients present with symptoms after the tumour has spread to other organs, making it very difficult to treat. Recent research suggests that genetic changes in pancreatic cancer cells that control metabolism and cellular calcium render these cells highly resistant to cell death. Therefore, our research focuses on understanding the metabolic changes and the mechanisms that control cellular calcium that make pancreatic cancer cells resistant to cell death and how this might be exploited to protect normal cells from catastrophic cell death during pancreatitis.

There are two major overlapping projects currently ongoing in my lab:
1) Insulin protection of pancreatic acinar cells during pancreatitis. Funded by the Medical Research Council (MRC; http://www.mrc.ac.uk/)

  2) Metabolic regulation of the PMCA in pancreatic cancer cells: Strategy for cell survival or “Achiles heel”. Funded by Pancreatic Cancer Research Fund http://www.pcrf.org.uk

These projects overlap in the context of the metabolic regulation of the PMCA in conferring a survival advantage during pancreatitis and pancreatic cancer. Consequently these projects involve collaborations with Prof Kaye Williams and Prof Ian Stratford (School of Pharmacy), Prof Michael Lisanti and Dr Cathy Tournier (Division of Molecular and Clinical Cancer), Prof Ajith Siriwardena (HPB Surgery, MRI) and Prof Roy Goodacre (School of Chemistry, Manchester Interdisciplinary Biocentre).