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Many diseases in humans, including cancers, are caused by genetic errors starting from a single cell. The origin of these genetic errors and the expansion of the abnormal cells carrying these genetic errors are often modelled as stochastic processes.

Dr Weini Huang, a Reader in the Centre for Complex Systems, and her PhD student Ms Elisa Scanu have developed a general framework to model the dynamics of cancer cells carrying multiple types of extrachromosomal DNA (ecDNA), a genetic error found in more than 30% of tumour samples across various cancer types and correlated to the worst clinical outcomes.

They apply this theoretical framework, based on branching processes, to different biological contexts, where ecDNA copies in the same cell may have distinct oncogenes (species), the same oncogenes but different mutations (genotypes), or different functions without any genetic changes (phenotypes). Their application in ecDNA species is part of a collaborative work with colleagues from the Medical School at Stanford University and has been recently published in Nature: full article here.