Dr Allinson's work is aimed at gaining a better understanding of how cells respond to DNA damage. The two main areas of her research are (i) understanding how skin cells respond to damage caused by ultraviolet radiation and (ii) the mechanisms underlying the repair of breaks in the DNA backbone and factors that might affect their efficiency.
Dr Cha’s group studies the molecular and cellular basis of ATM/ATR protein function. ATM and ATR are evolutionarily conserved signal transduction proteins found in all eukaryotes examined to date (e.g. yeasts, plants, insects, and mammals). They are involved in a range of fundamental processes including genome duplication, DNA damage response, cell cycle regulation, meiosis, and metabolism. In humans, loss of ATM- or ATR-function leads to the genetic disorder Ataxia-Telangiectasia (A-T) or Seckle syndrome, respectively. A-T and Seckle syndrome are rare and progressive childhood diseases characterized by cerebella ataxia, predisposition to cancer, diabetes, immune system defect, and/or microcephaly. They utilise a genetic model organism S. cerevisiae to study the molecular mechanisms of ATM/ATR function. The ultimate aim is to utilise findings of the study to devise an effective means to prevent and/or combat the devastating effects associated with A-T and Seckle syndrome.
One of the keys to understanding lifelong health is to understand the signalling pathways that operate inside cells and govern key fate decisions such as cell death, cell survival, cell division or cell senescence (collectively cell longevity). These signalling pathways involve enzymes called ‘protein kinases’ that attach phosphate groups to specific cellular proteins, thereby controlling their activity, location or abundance. In this way protein kinases orchestrate the cellular response to growth factor, nutrient factors, nutrient availability or stress and damage. Ageing results in part from the imbalance between cellular damage, accrued throughout life, and the progressive decline in stress response and repair pathways.
Dr Cook’s research group is interested in how protein kinases function in stress responses, the removal of damaged cellular components and the control of cellular lifespan. They believe this will enhance our understanding of how the normal declines in these processes drive ageing. Signalling pathways are frequently de-regulated in certain age-related diseases – notably in cancer, inflammation and neurodegeneration – and many protein kinases are attractive drug targets. Consequently, basic knowledge of signalling is translated through collaborations with charities and pharmaceutical companies (e.g. AstraZeneca and MISSION Therapeutics).
Prof Cox obtained her Phd from University College London in 1991 and during her early career she researched the role of common genetic factors in inflammatory diseases. For the last 15 years she has been using genetic epidemiology to identify genes that may be important susceptibility or survival factors for various cancers, in population-based and family-based studies. The hypotheses Prof Cox’s group is testing are mainly concerned with genes whose proteins are involved in the DNA damage response and apoptosis pathways, in collaboration with colleagues in the Academic Unit of Molecular Oncology. The aim is to determine the mechanisms of action of the genes to lead towards novel drug targets and improved risk modelling. They participate in several international genetics consortia including BCAC, PRACTICAL and COGs. Prof Cox’s current research is funded by the National Cancer Institute (NCI), Yorkshire Cancer Research (YCR), Cancer Research-UK (CR-UK) and Breast Cancer Now (BCN).
Main research interests are the mechanisms that maintain genome stability, in particular the cellular responses to DNA damage and DNA replication stress. Using Xenopus cell-free egg extracts as a model system, the primary aim of this work is a greater understanding of the way the various DNA damage response pathways are integrated with the cell cycle machinery and how failure of these pathways can contribute to the development and progression of cancer.
Having obtained a Doctor of Philosophy for studies investigating the immunomodulatory properties of human placental protein 14 from Sheffield City Polytechnic (now Sheffield Hallam University) in 1988, Professor Pockley undertook a two-year postdoctoral fellowship studying ocular mucosal immunoregulation in the Department of Immunology and Microbiology at Wayne State University, Detroit, USA. In January 1990, he returned to the UK to take up a Lectureship and direct the experimental transplantation programme in the Professorial Surgical Unit at the Medical College of St. Bartholomew´s Hospital, London. He returned to Sheffield as a Lecturer in September 1994, and was promoted to Reader in Immunobiology in 1996 and Professor of Immunobiology in 2004.
Professor Pockley was the recipient of a Yorkshire Enterprise Fellowship (2009-2010), the aim of which was to deliver training in Entrepreneurship and Commercial Exploitation. The Fellowship complemented his previous experience with the commercial sector via research contracts with Biotechnology companies in Canada and was primarily focussed on the development of a global resource for flow cytometry and related techniques (www.chromocyte.com). This has been incorporated in the UK and was launched in July 2010. Professor Pockley's experience in these and associated areas positions him well for the provision of academic and commercial insight in areas relating to immunobiology, flow cytometry and cell analysis.
Professor Pockley became the Associate Director of the John van Geest Cancer Research Centre at Nottingham Trent University on 1 May 2012 and retains an Honorary Professorship in the Department of Oncology at The University of Sheffield.
Prof Prior is part of the Oncology, Membrane Traffic and Signaling grouping in the Physiological Laboratory and is also Director of the Biomedical Electron Microscopy Unit. His research is funded by the Wellcome Trust, the BBSRC and North West Cancer Research.
Main interests lie in understanding how subcellular location of signalling cascades regulates their outcomes. Cell signalling regulates key cellular functions including cell division, death, migration and differentiation and many pathways are controlled by Ras proteins. Mutations causing hyper-activation of Ras are potent promoters of cancer. Ras is used as a model system because all mammalian cells contain 3 almost identical versions of Ras: H-Ras, K-Ras and N-Ras. Despite this, these proteins are known to generate different biological outputs. One possible explanation for these differences lies in their different microlocalisation within the cell surface and internal organelles allowing them to access different pools of activators and downstream signalling molecules.
Professor Pritchard studied Medicine at Manchester University (BSc (1st class Hons) in Medical Biochemistry, 1988; MB.ChB. (with Hons), 1991). After junior hospital posts (MRCP (UK) 1994), he returned to the University of Manchester to study for a PhD (Digestive Disorders Foundation and MRC Clinical Research Training Fellowships). In 2000 he moved to the University of Liverpool as a clinical lecturer and in 2002 he was awarded an Advanced Fellowship for Clinicians from the Wellcome Trust. He was awarded the ASNEMGE Rising Star award in 2007 and the Sir Francis Avery Jones Research Medal of the British Society of Gastroenterology in 2008. He was appointed Clinical Senior Lecturer at the University of Liverpool in 2006, Professor in 2009 and Head of the Department of Gastroenterology in 2010.
His current research focuses upon host factors which influence the development of gastrointestinal cancers and neuroendocrine tumours, in particular the importance of apoptosis, NF-κB signalling and the gastrin family of peptides. He is also an honorary Consultant Gastroenterologist at Royal Liverpool University Hospital, where he is the clinical lead for the Liverpool European Neuroendocrine Tumour Society (ENETS) Centre of Excellence.
Dr Royle is an Associate Professor (Reader) and Senior Cancer Research UK Fellow at Warwick Medical School. Work in his lab is focused on understanding two cellular processes at the molecular level: mitosis and clathrin-mediated endocytosis. He completed his PhD at University of Cambridge and moved to the MRC Laboratory of Molecular Biology, Cambridge, UK for post-doctoral work. While at the LMB he discovered a new function for the membrane trafficking protein clathrin at the mitotic spindle. Steve started his own lab as a lecturer in 2006 at the Physiological Laboratory, University of Liverpool and moved to Warwick in 2013. Financial support is from Cancer Research UK, MRC and BBSRC.
Dr Owen Sansom is Deputy Director of the Beatson Institute for Cancer Research in Glasgow, UK. His lab investigates two types of epithelial tumour: colorectal and pancreatic cancers, which are the second and fifth most common causes of cancer death worldwide, respectively. Recent sequencing studies have highlighted the common mutational drivers of these cancers and the focus of Professor Sansom’s group is to model these within the mouse to identify novel markers of the disease as well as targets for therapy. Over the past 5 years, his work has defined potential new therapeutic targets for colorectal cancers lacking Apc and for resectable pancreatic cancer.
Chris Twelves is Professor of Clinical Cancer Pharmacology and Oncology and Head of Section of Oncology and Clinical Research at the Leeds Cancer Research UK Centre. He is a medical oncologist with a particular interest in new drug development and clinical pharmacology; his clinical practice has been in colorectal and breast cancer.
After training as an oncologist in London he was Senior Lecturer, then Reader, in Medical Oncology in Glasgow at the Beatson Oncology Centre before taking up his current post at the University of Leeds and St James’s Institute of Oncology.
Professor Twelves heads the Experimental Cancer Medicine Centre in Leeds and has been a member of the Cancer Research UK New Agents Committee and Chair of the New Drug Development Group of the EORTC. He has been involved in the development of several important new agents including capecitabine, and eribulin. Professor Twelves has a particular interest in early clinical trials and pharmacokinetics including intra-tumoural drug pharmacokinetics.
Professor Twelves has published over 200 papers in journals including the New England Journal of Medicine, Lancet and Journal of Clinical Oncology and spoken at numerous international meetings. He has also edited, or contributed to, several books including one on Phase I clinical trials and another on the design of Phase II clinical trials.