Computational modelling of cancerous mutations in the EGFR/ERK signalling pathway |
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| Authors: | Richard J Orton Michiel E Adriaens Amelie Gormand Oliver E Sturm Walter Kolch David R Gilbert |
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| Institution: | (1) Institute of Comparative Medicine, Faculty of Veterinary Medicine, University of Glasgow, Glasgow, G61 1QH, UK;(2) Bioinformatics Research Centre, Department of Computing Science, University of Glasgow, Glasgow, G12 8QQ, UK;(3) Department of Bioinformatics - BiGCaT, Maastricht University, Maastricht, The Netherlands;(4) Department of Experimental Medical Science, Faculty of Medicine, Lund University, Lund, Sweden;(5) St Jude Children's Research Hospital, Memphis, Tennessee, TN 38105, USA;(6) Beatson Institute for Cancer Research, Garscube Estate, Glasgow, G61 IBD, UK;(7) School of Information Systems, Computing and Mathematics, Brunel University, Uxbridge, Middlesex, UB8 3PH, UK |
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| Abstract: | Background The Epidermal Growth Factor Receptor (EGFR) activated Extracellular-signal Regulated Kinase (ERK) pathway is a critical cell
signalling pathway that relays the signal for a cell to proliferate from the plasma membrane to the nucleus. Deregulation
of the EGFR/ERK pathway due to alterations affecting the expression or function of a number of pathway components has long
been associated with numerous forms of cancer. Under normal conditions, Epidermal Growth Factor (EGF) stimulates a rapid but
transient activation of ERK as the signal is rapidly shutdown. Whereas, under cancerous mutation conditions the ERK signal
cannot be shutdown and is sustained resulting in the constitutive activation of ERK and continual cell proliferation. In this
study, we have used computational modelling techniques to investigate what effects various cancerous alterations have on the
signalling flow through the ERK pathway. |
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