Clonal evolution in cancer

Greaves, Mel; Maley, Carlo C.

doi:10.1038/nature10762

Cited by 2,731 publications

(2,469 citation statements)

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“…While it is now understood that cancer is a process of clonal selection [Cairns 1975, Nowell 1976, Crespi & Summers 2005, Merlo et al 2006, Greaves & Maley 2012, and game theory has often been mentioned as a relevant for cancer research [Gatenby & Maini 2003, Merlo et al 2006, Axelrod et al 2006, Lambert et al 2011, the study of growth factors in the framework of evolutionary game theory is still limited. Tomlinson [1997] and Tomlinson & Bodmer [1997] used the hawk-dove game, to explain why game theory can be used to understand conflict and cooperation between cancer cells; subsequent papers [Bach et al 2001, Dingli et al 2009, Basanta et al 2008a,b, 2011, 2012, Gerstung et al 2011 have extended that model to up to 4 strategies.…”

Section: Further Developments Of the Modelmentioning

confidence: 99%

Cooperation among cancer cells as public goods games on Voronoi networks

Archetti

2016

Journal of Theoretical Biology

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Cancer cells produce growth factors that diffuse and sustain tumor proliferation, a form of cooperation among cancer cells that can be studied using mathematical models of public goods in the framework of evolutionary game theory. Cell populations, however, form heterogeneous networks that cannot be described by regular lattices or scale-free networks, the types of graphs generally used in the study of cooperation. To describe the dynamics of growth factor production in populations of cancer cells, I study public goods games on Voronoi networks, using a range of non-linear benefits that account for the known properties of growth factors, and different types of diffusion gradients. The results are surprisingly similar to those obtained on regular graphs and different from results on scale-free networks, revealing that network heterogeneity per se does not promote cooperation when public goods diffuse beyond one-step neighbours. The exact shape of the diffusion gradient is not crucial, however, whereas the type of non-linear benefit is an essential determinant of the dynamics. Public goods games on Voronoi networks can shed light on intra-tumor heterogeneity, the evolution of resistance to therapies that target growth factors, and new types of cell therapy.

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Section: Further Developments Of the Modelmentioning

confidence: 99%

Cooperation among cancer cells as public goods games on Voronoi networks

Archetti

2016

Journal of Theoretical Biology

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“…Labeling of individual cell clones and modeling of their in vivo expansion can facilitate the understanding of clonal development and adaptation during tumor progression within the heterogeneous landscape in cancer. 1,2 Furthermore, the ability to label and trace individual cells is demanded in many other research areas, including stem cell biology, neuronal networks, or testing of advanced biologicals like oncolytic viruses. Unfortunately, in vivo tracking of single-cell clones has been technically challenging.…”

Section: Introductionmentioning

confidence: 99%

Optical Barcoding for Single-Clone Tracking to Study Tumor Heterogeneity

et al. 2017

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Intratumoral heterogeneity has been identified as one of the strongest drivers of treatment resistance and tumor recurrence. Therefore, investigating the complex clonal architecture of tumors over time has become a major challenge in cancer research. We developed a new fluorescent "optical barcoding" technique that allows fast tracking, identification, and quantification of live cell clones in vitro and in vivo using flow cytometry (FC). We optically barcoded two cell lines derived from malignant glioma, an exemplary heterogeneous brain tumor. In agreement with mathematical combinatorics, we demonstrate that up to 41 clones can unambiguously be marked using six fluorescent proteins and a maximum of three colors per clone. We show that optical barcoding facilitates sensitive, precise, rapid, and inexpensive analysis of clonal composition kinetics of heterogeneous cell populations by FC. We further assessed the quantitative contribution of multiple clones to glioblastoma growth in vivo and we highlight the potential to recover individual viable cell clones by fluorescence-activated cell sorting. In summary, we demonstrate that optical barcoding is a powerful technique for clonal cell tracking in vitro and in vivo, rendering this approach a potent tool for studying the heterogeneity of complex tissues, in particular, cancer.

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“…In clonal evolution model, tumors are characterized by stochastic mutation and initial sensitivity to RT. After RT exposure, the fittest subpopulations survive under selective pressure [38], leading to tumor subclone repopulation and gradual development of resistance. RT itself also induces mutations, thus may endow some populations with radiation resistance.…”

Section: Discussionmentioning

confidence: 99%

Oncogenic transformation of normal breast epithelial cells co-cultured with cancer cells

Song

Zhou

et al. 2018

Cell Cycle

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The heterogeneity in human breast cancer poses a challenge for effective treatment. Better understanding of tumor initiation and development will help to resolve this problem. Current models explaining intratumoral diversity include cancer stem cells, clonal evolution and cancer cell dedifferentiation and reprogramming. Herein, a new model, cancer transmission, is proposed to explain cancer heterogeneity. We found breast cancer cells (MCF10A.NeuT) were capable of transforming normal mammary epithelial cells (MCF10A). The transformed cells exhibited cancerous properties including enhanced proliferation and migration, loss of apical-basal polarity and depolarized acini structure associated with epithelial-mesenchymal transition (EMT). The transformed MCF10A cells displayed distinct EMT characteristics compared to parental cells. We further showed that cancer cell-secreted factors were sufficient to induce cancerous transformation of normal cells. Furthermore, transformed cells were resistant to radiation treatment, providing new insights into mechanisms underlying therapeutic resistance.

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Clonal evolution in cancer

Cited by 2,731 publications

References 100 publications

Cooperation among cancer cells as public goods games on Voronoi networks

Cooperation among cancer cells as public goods games on Voronoi networks

Optical Barcoding for Single-Clone Tracking to Study Tumor Heterogeneity

Oncogenic transformation of normal breast epithelial cells co-cultured with cancer cells

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