Catrin Pritchard

C Pritchard

Tel: +44 (0)116 229 7061


Personal details

  • 1983-1987: PhD at the Imperial Cancer Research Fund
  • 1987-1990: Postdoctoral fellow, University of California, San Francisco, USA
  • 1991-1994: Postdoctoral fellow, DNAX Research Institute, Palo Alto, California, USA
  • 1994-2005: Royal Society Research University Research Fellow, University of Leicester
  • 2005-2006: Lecturer, Department of Biochemistry, University of Leicester
  • 2006-2007: Reader, Department of Biochemistry, University of Leicester
  • 2009: Professor of Cancer Biochemistry, University of Leicester
  • 2010: Royal Society-Wolfson Research Merit Award Holder
  • 2011: Cancer Theme Lead
  • 2014: Science Director Cancer Research UK Leicester Centre


RAF/MEK/ERK signalling in normal and cancer cells

Cells are able to respond to their extracellular environment by transducing signals received at the membrane through cascades of intracellular proteins to physiological effectors. These intracellular signal transduction pathways serve to control key cellular processes including cell proliferation, differentiation, programmed cell death, changes in cell shape and motility, and manifestation of the tumour phenotype.

Central to many of these pathways are MAP kinase modules, the archetypal form of which is a cascade of sequentially acting protein kinases named RAF, MEK1/2 and ERK1/2 that are activated downstream of cell surface receptors and the RAS GTPases.

Fig. 1a.jpg

We are analysing the role of the RAF serine/threonine protein kinases that comprise a family of three related genes in mammals: ARAF, BRAF and CRAF. The RAF proteins have been identified as critical signalling intermediates between RAS and ERKs and they are thought to mediate many of the proliferative effects and cell shape changes induced by oncogenic RAS in tumour cells.

In addition, a sequencing screen of cancer samples has revealed activating mutations of the BRAF gene in ~70% of human malignant melanomas and 15% of colorectal cancers. The vast majority of these mutations give rise to a mutant version of BRAF encoding a valine to glutamic acid change at residue 600 (V600E) that gives rise to increased BRAF kinase activity, constitutive ERK activation and transformation.

Figure 2jpeg.jpg

Research in our laboratory focusses on two major areas:

  • Understanding how mutant versions of oncogenic BRAF initiate and drive human cancer development
  • Understanding the mechanisms by which the three RAF proteins control output of the MEK/ERK pathway

We use a range of state-of-the-art molecular and cell biology techniques including transgenic mouse models, proteomics, fluorescence microscopy, protein biochemistry and analysis of human tumour samples. We currently have projects in collaboration with the Paterson Institute, Manchester to explore the use of mouse models to identify novel therapeutic targets and biomarkers for V600EBRAF-driven cancers.

We are also working with the Babraham Institute to investigate the role of RAF subcellular localisation in determining the magnitude and duration of ERK activation.

Current funding

  • Cancer Research UK Programme Grant
  • Royal Society Wolfson Merit Award
  • Wellcome Trust Capital Investment Award
  • MRC Doctoral Training Grants to Ellie Karekla and Ricky Trigg
  • Cancer Research UK Leicester Centre Award

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Contact Details

Department of Molecular and Cell Biology
Henry Wellcome Building
Lancaster Road
LE1 7RH (Postal)

LE1 7HB (Sat Nav/Online maps)

T:  +44(0)116 229 7038
F:  +44(0)116 229 7123


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Redfearn Lecture 2017

To Be Confirmed