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BEYOND GENETIC DISCOVERY IN INFLAMMATORY BOWEL DISEASE
In-person only
The inflammatory bowel diseases, Crohn’s disease & ulcerative colitis are increasingly rapidly in incidence and prevalence throughout the World. Current projections estimate that 1.5 – 2.0 % of the population may be affected when prevalence equilibrium is reached in countries in Western Europe and North America.
Over the last 30 years, genetic studies have been highly successful, allowing the characterisation of genetic architecture of IBD; over 300 genetic loci have been implicated by GWAS studies allowing identification of pathways involved in pathogenesis, and targets for therapeutic intervention.
However, it is very clear that genetic factors contribute less than 30% disease variance – genetic variation alone fails to explain disease epidemiology or familial risk. The need to characterise gene-environmental interactions and the disease exposome is fundamental to understanding pathogenesis, and in turn to moving towards prevention.
We hypothesise that epigenetic mechanisms are likely to be critical in gene-environmental interactions – with well characterised effects of smoking, and of air pollution on DNA methylation providing catalysts for these studies.
Our studies over the last decade have taken advantage of technical advances in characterising the epigenome in health, in ageing and in disease; and have built on the known effects of the exposome on the circulating DNA methylome. Thus, we have characterised the circulating methylome in Crohn’s disease and ulcerative colitis in adults and children; we demonstrate a stable highly reproducible series of changes at diagnosis in inception cohorts across Northern Europe and characterise the influence of genetic and non-genetic factors in shaping the methylome. The findings provide further insights into disease pathogenesis. Early clinical applications include the potential for biomarkers in predicting disease susceptibilty, in diagnosis, and in stratification for therapy. Excitingly, causal inference analysis using genetic and epigenetic data allow identification of a series of molecular pathways involved in the effects of the exposome on disease.
Date:
19 January 2026, 12:00
Venue:
Kennedy Institute of Rheumatology, Headington OX3 7FY
Venue Details:
Kennedy Lecture Theatre
Speaker:
Professor Jack Satsangi (University of Oxford)
Organising department:
Kennedy Institute of Rheumatology
Organiser:
Tess Lawless (Kennedy Institute of Rheumatology)
Host:
Professor Fiona Powrie (Kennedy Institute of Rheumatlogy)
Part of:
Kennedy Institute Seminars
Booking required?:
Not required
Audience:
Members of the University only
Editor:
Theresa Lawless
