Non-cell-autonomous driving of tumour growth supports sub-clonal heterogeneity

Andriy Marusyk, Doris P. Tabassum, Philipp M. Altrock, Vanessa Almendro, Franziska Michor and Kornelia Polyak ()
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Andriy Marusyk: Dana-Farber Cancer Institute
Doris P. Tabassum: Dana-Farber Cancer Institute
Philipp M. Altrock: Dana-Farber Cancer Institute
Vanessa Almendro: Dana-Farber Cancer Institute
Franziska Michor: Dana-Farber Cancer Institute
Kornelia Polyak: Dana-Farber Cancer Institute

Nature, 2014, vol. 514, issue 7520, 54-58

Abstract: Abstract Cancers arise through a process of somatic evolution that can result in substantial sub-clonal heterogeneity within tumours. The mechanisms responsible for the coexistence of distinct sub-clones and the biological consequences of this coexistence remain poorly understood. Here we used a mouse xenograft model to investigate the impact of sub-clonal heterogeneity on tumour phenotypes and the competitive expansion of individual clones. We found that tumour growth can be driven by a minor cell subpopulation, which enhances the proliferation of all cells within a tumour by overcoming environmental constraints and yet can be outcompeted by faster proliferating competitors, resulting in tumour collapse. We developed a mathematical modelling framework to identify the rules underlying the generation of intra-tumour clonal heterogeneity. We found that non-cell-autonomous driving of tumour growth, together with clonal interference, stabilizes sub-clonal heterogeneity, thereby enabling inter-clonal interactions that can lead to new phenotypic traits.

Date: 2014
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DOI: 10.1038/nature13556

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