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Wound healing and cancer

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In our lab we investigate fundamental aspects of tissue repair, including re-epithelialisation and connective-tissue contraction, using several model organisms, from Drosophila through to mice, with the end goal of developing therapeutics to speed up healing and prevent scarring. To study the wound inflammatory response we have established models of inflammation in the Drosophila embryo and in the translucent zebrafish larva, which allow us to make movies of leukocyte migration into the wound and to dissect the genetics of inflammatory cell recruitment towards tissue damage. We have also utilized array approaches in both flies and mice that are deficient in inflammatory cells, to determine inflammation-dependent versus -independent gene inductions upon wounding. One such inflammation-dependent, wound-expressed gene is osteopontin and we find that if this gene is "knocked-down" at the wound site, then repair is faster and scarring is significantly reduced.  Recently we have begun investigating parallels between wound healing and cancer. Just as for wounds, we find H2O2 to be the key attractant enabling immune cells to sense early clones of transformed cells before they progress to cancers. We find that clones of transformed cells deprived of immune cells proliferate at a slower rate suggesting that trophic signals, which we have now shown to include prostaglandins, are delivered to the transformed cells by immune cells.

This area contributes to the wider Cell Signalling and Biology research theme within the School of Physiology and Pharmacology.