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Haughey, M. J.

Publications and source records attributed to Haughey, M. J..

2 recordsLinked to original sources

First passage time analysis of spatial mutation patterns reveals evolutionary dynamics of pre-existing resistance in colorectal cancer

The footprint left by early cancer dynamics on the spatial arrangement of tumour cells is poorly understood, and yet could encode information about how therapy resistant sub-clones grew within the expanding tumour. Novel methods of quantifying spatial tumour data at the cellular scale are required to link evolutionary dynamics to the resulting spatial architecture of the tumour. Here, we propose a framework using first passage times of random walks to quantify the complex spatial patterns of tumour cell population mixing. First, using a toy model of cell mixing we demonstrate how first passage time statistics can distinguish between different pattern structures. We then apply our method to simulated patterns of wild-type and mutated tumour cell population mixing, generated using an agent-based model of expanding tumours, to explore how first passage times reflect mutant cell replicative advantage, time of emergence and strength of cell pushing. Finally, we analyse experimentally measured patterns of genetic point mutations in human colorectal cancer, and estimate parameters of early sub-clonal dynamics using our spatial computational model. We uncover a wide range of mutant cell replicative advantages and timings, with the majority of sampled tumours consistent with boundary driven growth or short-range cell pushing. By analysing multiple sub-sampled regions in a small number of samples, we explore how the distribution of inferred dynamics could inform about the initial mutational event. Our results demonstrate the efficacy of first passage time analysis as a new methodology for quantifying cell mixing patterns in vivo, and suggest that patterns of sub-clonal mixing can provide insights into early cancer dynamics.

cancer biology↗

Clonal dynamics of normal hepatocyte expansions in homeostatic human livers and their association with the biliary epithelium

The majority of human liver research is disease-focused such that far less is known of cellular dynamics within normal human liver. We have leveraged cytochrome c oxidase deficiency as a marker of clonal hepatocyte populations in such tissues. We demonstrate these populations commonly associate with portal tracts and lineage-trace hepatocytes with cholangiocytes, indicating the presence of a bipotential common ancestor at this niche. We also observe rare periportal SOX9+ hepatocytes progenitor candidates in our human tissues. To understand clonal expansion dynamics, we measured methylation diversity and identified mtDNA variants by next-generation sequencing within spatially-defined clonal hepatocyte patches. We coupled our sequencing with mathematical modelling and Bayesian inference to compare spatial patterns of mtDNA variants under assumptions with or without faster expansion from a portal-associated niche. These datasets support the existence of a periportal progenitor niche and indicate that clonal patches slowly expand, perhaps due to acute environmental stimuli, then quiesce. These findings crucially contribute to our understanding of hepatocyte dynamics in normal human liver and provide a baseline for understanding how such dynamics may be modulated in diseased liver.

cell biology↗