ArticleCell proliferation2008
A quantitative study of growth variability of tumour cell clones in vitro.
Article in Cell proliferation, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- LeafRank: A phylodynamic framework for inferring relative fitness from single-cell phylogenies in chromosomally unstable tumors.bioRxiv : the preprint server for biology · 2026Article
- Article
- Article
- Bioactivity of the Murex Homeopathic Remedy and of Extracts from an Australian Muricid Mollusc against Human Cancer Cells.Evidence-based complementary and alternative medicine : eCAM · 2011Article
- Microplate spectrophotometry for high-throughput screening of cytotoxic molecules.Cell proliferation · 2010Article
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectivesIn this study, we quantify growth variability of tumour cell clones from a human leukaemia cell line. MATERIALS AND
methodsWe have used microplate spectrophotometry to measure growth kinetics of hundreds of individual cell clones from the Molt3 cell line. Growth rate of each clonal population has been estimated by fitting experimental data with the logistic equation.
resultsGrowth rates were observed to vary between different clones. Up to six clones with growth rates above or below mean growth rate of the parent population were further cloned and growth rates of their offspring were measured. Distribution of growth rates of the subclones did not significantly differ from that of the parent population, thus suggesting that growth variability has an epigenetic origin. To explain observed distributions of clonal growth rates, we have developed a probabilistic model, assuming that fluctuation in the number of mitochondria through successive cell cycles is the leading cause of growth variability. For fitting purposes, we have estimated experimentally by flow cytometry the average maximum number of mitochondria in Molt3 cells. The model fits nicely observed distributions in growth rates; however, cells in which mitochondria were rendered non-functional (rho(0) cells) showed only 30% reduction in clonal growth variability with respect to normal cells.
conclusionsA tumour cell population is a dynamic ensemble of clones with highly variable growth rates. At least part of this variability is due to fluctuations in the initial number of mitochondria in daughter cells.
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