Jean-christophe Bourdon

Biography

Dr. Jean-Christophe Bourdon did his PhD research project on p53 under the co-supervision of Prof Brigitte Debuire and Dr Evelyne and Pierre May, co-discoverer of p53. He earned his Ph.D in Cellular and Molecular Biology in 1997 at Paris XI University, France. Dr Bourdon joined in 1998 David Lane's lab, co-discoverer of p53 at the University of Dundee, Scotland. He became University Senior Research Fellow in 2005 and co-director of the Inserm-European Associated Laboratory, co-directed by Dr Anne-Catherine Prats (Toulouse University, France) in 2006. In April 2010, he was appointed Senior Lecturer at the College of Medicine at Dundee University, position that he presently held. In June 2012, he was awarded the prestigious fellowship from Breast Cancer Campaign.

Research Interest

Dr Bourdon established during his Ph.D in 1997 that p53 responsive elements are composed of clusters of DNA sequence RRRCWWGYYY. He validated this consensus sequence for p53 response element by identifying several p53 target genes. Joining the David Lane’s laboratory, he characterised a new p53-inducible pro-apoptotic gene that he named Scotin (also named Shisa-5). Scotin is a transmembrane protein that triggers apoptosis in a caspase dependent manner in response to DNA damage and Endoplasmic reticulum stress. Dr Bourdon demonstrated that the human p53 gene encodes 12 different p53 protein isoforms (containing different domains) due to alternative splicing, alternative initiation of translation and alternative promoter usage (1) and that the dual gene structure of the p53 gene family is conserved through evolution from Drosophila to man. His research group demonstrated that p53 isoforms are associated with cancer patient prognosis. They established that p53 isoforms regulate cell response to damage modulating cell cycle progression, senescence, differentiation, cell death, angiogenesis, endothelial and tumour cell migration. The aims of his research group are 1- to characterise the biological activities of the p53 isoforms in cancer, particularly in breast cancer, 2- to establish regulation of p53 isoforms expression at the mRNA (splicing, internal promoter) and protein levels (proteasome degradation), 3- to define p53 isoform as predictive treatment biomarkers (personalised treatment) and 4- to develop new drugs that  modulate p53 protein isoform expression in order to control cell response to cancer treatment.