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Paul Martin Overview

Professor Martin's lab is investigating parallels between cancer and wound repair. In particular, they are interested in epigenetic changes that may "unsilence" wound repair genes following tissue damage and thus enable the cell migration and proliferative responses needed for healing.

They have reported a reciprocal up and down regulation of the polycombs (Eed, Ezh2, and Suz12) and their associated, newly described, demethylases (Jmjd3 and Utx), which result in a loss of repressive histone H3 lysine 27 trimethylation (H3K27me3) marks in the wound epidermis and a consequent upregulation of several target wound genes eg EGFR and myc (Shaw and Martin, 2009, EMBO R 10, 881-6). These effects are transient and return to normal when the wound has healed. Next steps are to analyse what is upstream of this polycomb downregulation ie what regulates the regulators upon wounding, and they are also searching for more repair genes that might be unsilenced in a similar fashion. Clearly, because there is much overlap between the repair transcriptome and those genes that form part of many cancer transcriptional "signatures", it is very important that these genes are tightly regulated during the wound repair process. Several cancers that are often associated with chronic non-healing wounds are known, and so an understanding of these episodes may guide in the design of both tissue repair and cancer therapeutics.