Speaker
Description
Histologically homogenous tumours often hide distinct genetic subpopulations called subclones. These often come about due to mutations and structural variations of particular driver genes that seem to lead to a rapid acceleration of growth, but do not become fully clonal, perhaps not sufficiently fit to outcompete the rest of the population. The recent expansion of spatial transcriptomics has allowed for further study of these clonal dynamics.
We have developed a new model of the tumour with an invasive front that picks up driver mutations as it progresses through the surrounding tissue, generalising earlier geometric models. We can describe the process of invasion and growth using a simple variational principle, while the model itself is complex enough to describe cells growing at speeds that vary with their microenvironment and genetics. Using spatial transcriptomic data, we can also validate the model, analyse driver events, and quantify the relative speed of different driver events, allowing for insight into the in vitro behaviour of these drivers.
