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. 2014 Dec 10;47(1):66. doi: 10.1186/0717-6287-47-66

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© Fulawka et al.; licensee BioMed Central. 2014

This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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Basic tumour heterogeneity models. A - Clonal evolution model. High proliferation and genomic instability result in a large number of cells differing in genotype and thus phenotype. The best fitted cells are selected by Darwinian processes to generate clonal variants of the tumour. B - Cancer stem cell model. CSC population is capable of unlimited number of divisions. Tumour heterogeneity results from existence of phenotypically diverse populations of different stages of cell maturation.