Heritable tumor cell division rate heterogeneity induces clonal dominance

Tumors consist of a hierarchical population of cells that differ in their phenotype and genotype. This hierarchical organization of cells means that a few clones (i.e., cells and several generations of offspring) are abundant while most are rare, which is called clonal dominance. Such dominance also...

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Vydáno v:PLoS computational biology Ročník 14; číslo 2; s. e1005954
Hlavní autoři: Palm, Margriet M., Elemans, Marjet, Beltman, Joost B.
Médium: Journal Article
Jazyk:angličtina
Vydáno: United States Public Library of Science 01.02.2018
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ISSN:1553-7358, 1553-734X, 1553-7358
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Abstract Tumors consist of a hierarchical population of cells that differ in their phenotype and genotype. This hierarchical organization of cells means that a few clones (i.e., cells and several generations of offspring) are abundant while most are rare, which is called clonal dominance. Such dominance also occurred in published in vitro iterated growth and passage experiments with tumor cells in which genetic barcodes were used for lineage tracing. A potential source for such heterogeneity is that dominant clones derive from cancer stem cells with an unlimited self-renewal capacity. Furthermore, ongoing evolution and selection within the growing population may also induce clonal dominance. To understand how clonal dominance developed in the iterated growth and passage experiments, we built a computational model that accurately simulates these experiments. The model simulations reproduced the clonal dominance that developed in in vitro iterated growth and passage experiments when the division rates vary between cells, due to a combination of initial variation and of ongoing mutational processes. In contrast, the experimental results can neither be reproduced with a model that considers random growth and passage, nor with a model based on cancer stem cells. Altogether, our model suggests that in vitro clonal dominance develops due to selection of fast-dividing clones.
AbstractList Tumors consist of a hierarchical population of cells that differ in their phenotype and genotype. This hierarchical organization of cells means that a few clones (i.e., cells and several generations of offspring) are abundant while most are rare, which is called clonal dominance. Such dominance also occurred in published in vitro iterated growth and passage experiments with tumor cells in which genetic barcodes were used for lineage tracing. A potential source for such heterogeneity is that dominant clones derive from cancer stem cells with an unlimited self-renewal capacity. Furthermore, ongoing evolution and selection within the growing population may also induce clonal dominance. To understand how clonal dominance developed in the iterated growth and passage experiments, we built a computational model that accurately simulates these experiments. The model simulations reproduced the clonal dominance that developed in in vitro iterated growth and passage experiments when the division rates vary between cells, due to a combination of initial variation and of ongoing mutational processes. In contrast, the experimental results can neither be reproduced with a model that considers random growth and passage, nor with a model based on cancer stem cells. Altogether, our model suggests that in vitro clonal dominance develops due to selection of fast-dividing clones.
Tumors consist of a hierarchical population of cells that differ in their phenotype and genotype. This hierarchical organization of cells means that a few clones (i.e., cells and several generations of offspring) are abundant while most are rare, which is called clonal dominance. Such dominance also occurred in published in vitro iterated growth and passage experiments with tumor cells in which genetic barcodes were used for lineage tracing. A potential source for such heterogeneity is that dominant clones derive from cancer stem cells with an unlimited self-renewal capacity. Furthermore, ongoing evolution and selection within the growing population may also induce clonal dominance. To understand how clonal dominance developed in the iterated growth and passage experiments, we built a computational model that accurately simulates these experiments. The model simulations reproduced the clonal dominance that developed in in vitro iterated growth and passage experiments when the division rates vary between cells, due to a combination of initial variation and of ongoing mutational processes. In contrast, the experimental results can neither be reproduced with a model that considers random growth and passage, nor with a model based on cancer stem cells. Altogether, our model suggests that in vitro clonal dominance develops due to selection of fast-dividing clones.Tumors consist of a hierarchical population of cells that differ in their phenotype and genotype. This hierarchical organization of cells means that a few clones (i.e., cells and several generations of offspring) are abundant while most are rare, which is called clonal dominance. Such dominance also occurred in published in vitro iterated growth and passage experiments with tumor cells in which genetic barcodes were used for lineage tracing. A potential source for such heterogeneity is that dominant clones derive from cancer stem cells with an unlimited self-renewal capacity. Furthermore, ongoing evolution and selection within the growing population may also induce clonal dominance. To understand how clonal dominance developed in the iterated growth and passage experiments, we built a computational model that accurately simulates these experiments. The model simulations reproduced the clonal dominance that developed in in vitro iterated growth and passage experiments when the division rates vary between cells, due to a combination of initial variation and of ongoing mutational processes. In contrast, the experimental results can neither be reproduced with a model that considers random growth and passage, nor with a model based on cancer stem cells. Altogether, our model suggests that in vitro clonal dominance develops due to selection of fast-dividing clones.
Tumors consist of a hierarchical population of cells that differ in their phenotype and genotype. This hierarchical organization of cells means that a few clones (i.e., cells and several generations of offspring) are abundant while most are rare, which is called clonal dominance. Such dominance also occurred in published in vitro iterated growth and passage experiments with tumor cells in which genetic barcodes were used for lineage tracing. A potential source for such heterogeneity is that dominant clones derive from cancer stem cells with an unlimited self-renewal capacity. Furthermore, ongoing evolution and selection within the growing population may also induce clonal dominance. To understand how clonal dominance developed in the iterated growth and passage experiments, we built a computational model that accurately simulates these experiments. The model simulations reproduced the clonal dominance that developed in in vitro iterated growth and passage experiments when the division rates vary between cells, due to a combination of initial variation and of ongoing mutational processes. In contrast, the experimental results can neither be reproduced with a model that considers random growth and passage, nor with a model based on cancer stem cells. Altogether, our model suggests that in vitro clonal dominance develops due to selection of fast-dividing clones. Tumors consist of numerous cell populations, i.e., clones, that differ with respect to genotype, and potentially with respect to phenotype, and these populations strongly differ in their size. A limited number of clones tend to dominate tumors, but it remains unclear how this clonal dominance arises. Potential driving mechanisms are the presence of cancer stem cells, which either divide indefinitely of differentiate into cells with a limited division potential, and ongoing evolutionary processes within the tumor. Here we use a computational model to understand how clonal dominance developed during in vitro growth and passage experiments with cancer cells. Incorporating cancer stem cells in this model did not result in a match between simulations and in vitro data. In contrast, by considering all cells to divide indefinitely and division rates to evolve due to the combination of division rate variability and selection by passage, our model closely matches the in vitro data.
Audience Academic
Author Elemans, Marjet
Beltman, Joost B.
Palm, Margriet M.
AuthorAffiliation Division of Drug Discovery and Safety, Leiden Academic Center for Drug Research, Leiden University, Leiden, The Netherlands
University of California Irvine, UNITED STATES
AuthorAffiliation_xml – name: University of California Irvine, UNITED STATES
– name: Division of Drug Discovery and Safety, Leiden Academic Center for Drug Research, Leiden University, Leiden, The Netherlands
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  givenname: Margriet M.
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  surname: Palm
  fullname: Palm, Margriet M.
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  surname: Elemans
  fullname: Elemans, Marjet
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  givenname: Joost B.
  surname: Beltman
  fullname: Beltman, Joost B.
BackLink https://www.ncbi.nlm.nih.gov/pubmed/29432417$$D View this record in MEDLINE/PubMed
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ContentType Journal Article
Copyright COPYRIGHT 2018 Public Library of Science
2018 Public Library of Science. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited: Palm MM, Elemans M, Beltman JB (2018) Heritable tumor cell division rate heterogeneity induces clonal dominance. PLoS Comput Biol 14(2): e1005954. https://doi.org/10.1371/journal.pcbi.1005954
2018 Palm et al 2018 Palm et al
2018 Public Library of Science. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited: Palm MM, Elemans M, Beltman JB (2018) Heritable tumor cell division rate heterogeneity induces clonal dominance. PLoS Comput Biol 14(2): e1005954. https://doi.org/10.1371/journal.pcbi.1005954
Copyright_xml – notice: COPYRIGHT 2018 Public Library of Science
– notice: 2018 Public Library of Science. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited: Palm MM, Elemans M, Beltman JB (2018) Heritable tumor cell division rate heterogeneity induces clonal dominance. PLoS Comput Biol 14(2): e1005954. https://doi.org/10.1371/journal.pcbi.1005954
– notice: 2018 Palm et al 2018 Palm et al
– notice: 2018 Public Library of Science. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited: Palm MM, Elemans M, Beltman JB (2018) Heritable tumor cell division rate heterogeneity induces clonal dominance. PLoS Comput Biol 14(2): e1005954. https://doi.org/10.1371/journal.pcbi.1005954
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Snippet Tumors consist of a hierarchical population of cells that differ in their phenotype and genotype. This hierarchical organization of cells means that a few...
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SubjectTerms Autosomal dominant inheritance
Bar codes
Bioinformatics
Biology and Life Sciences
Cancer
Cell division
Cell self-renewal
Computer applications
Computer simulation
Dominance
Epigenetics
Experiments
Gene expression
Genetic aspects
Genotypes
Health aspects
Heterogeneity
Labeling
Medicine and Health Sciences
Mutation
Offspring
Phenotypes
Physiological aspects
R&D
Research & development
Research and Analysis Methods
Software
Stem cells
Tumor cells
Tumors
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Title Heritable tumor cell division rate heterogeneity induces clonal dominance
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Volume 14
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