Aging tissues and carcinogenesis
As tissues age, cells accumulate mutations that change the activity of proteins. These changes may alter how the cells grow and compete in the tissue, enabling clones to persist and expand by increasing their fitness. Over time these clones may colonise the tissue, only to stop or regress as they meet alternative clones of similar or greater fitness. This process of expansion and regression may occur several times over a lifetime. Fit clones are however not necessarily cancer progressing, but may contain the seeds of cancer.
My group uses computational biology to study the impact of mutations on cells, from how it changes the activity of individual proteins, to how it alters the phenotype of the cell, to the competition of cells in a tissue. Through understanding the effect of mutation we hope to identify new routes to patient stratification and therapy.
Dr Ben Hall is a computational biologist and Royal Society Research Fellow in the department of medical physics and biomedical engineering, at UCL. He leads a program on “Modelling the decision processes of cancer”, where his team develop computational models of the aging tissue and carcinogenesis. He holds a Royal Society University Research Fellowship, and work in his group is funded by the MRC, Microsoft Research, and the Royal Society.
Prior to his current position he worked as an MRC Investigator, leading a programme at the MRC Cancer Unit in the University of Cambridge. Before that he worked with Dr Jasmin Fisher at Microsoft, constructing executable models of organ development in C. elegans and developing tools for formal verification in biology. He completed his DPhil and previous post-doctoral positions in molecular modelling at Oxford and UCL.