Understanding how our DNA affects our risk of developing bowel cancer
More than 1 in 20 people will develop bowel cancer in their lifetime. We know that some people have an increased risk of developing cancer due to small differences in their DNA (common genetic variants). What we don’t yet know is why some variations increase the risk while others do not, and it is important to discover what these variants do and how they increase cancer development.
Most variants do not even change the coding sequence of genes or the type of protein they produce. Instead, they change how much gene product is produced, or when and where in the body it is turned on.
Targeting two specific variations to increase our understanding of genetic triggers for bowel cancer
This PhD will investigate two groups of bowel cancer risk variants in neighbouring genes. POLD3 is important for copying and repairing DNA and CHRDL2 helps maintain normal bowel cells, two things that often go wrong in bowel cancers. So far, no-one knows how changing the amount of POLD3 and CHRDL2 increases cancer risk. This study will investigate if more POLD3 and CHRDL2 in tumours could affect a patient’s survival or treatment response. We will also study how the variants change the amount of gene product and how this affects cancer cells. Do they grow faster, live longer or gather more mutations?
The findings should help doctors choose the most suitable treatments for patients, and allow scientists to develop new cancer treatments. It could even lead, ultimately, to methods of bowel cancer screening that assess people’s risk of developing bowel cancer based on their genetic code – enabling greater vigilance of these individuals.
The research team
This PhD will be supervised by Dr Annabelle Lewis at Brunel University London