Evolutionary biology of cancer

Crespi, Bernard J.; Summers, Kyle

doi:10.1016/j.tree.2005.07.007

Cited by 232 publications

(188 citation statements)

References 80 publications

(140 reference statements)

Supporting

Mentioning

182

Contrasting

Unclassified

Order By: Relevance

“…Through this process, which occurs throughout the lifetime of a tumor, any cancer cell can potentially become invasive and cause metastasis or become resistant to therapies and cause recurrence. 13,25,[52][53][54][55][56] Supporting evidence. Nowell first proposed the clonal evolution model in 1976.…”

Section: The Cancer Stem Cell Hypothesismentioning

confidence: 92%

Breast Tumor Heterogeneity: Cancer Stem Cells or Clonal Evolution?

Campbell

Polyák²

2007

Cell Cycle

365

272

View full text Add to dashboard Cite

Breast tumors are composed of a variety of cell types with distinct morphologies and behaviors. It is not clear how this tumor heterogeneity comes about. Two popular concepts that attempt to explain this are the cancer stem cell hypothesis and the clonal evolution model. Each of these ideas has been investigated for some time, leading to the accumulation of numerous findings that are used to support one or the other. Although the two views share some similarities, they are fundamentally different notions with very different clinical implications. Analysis of the research backing each concept, along with a review of the results of our recent study investigating putative breast cancer stem cells, suggests how the cancer stem cell hypothesis and the clonal evolution model may be involved in generating breast tumor heterogeneity. An understanding of this process will allow the development of more effective ways to treat and prevent breast cancer.

show abstract

Section: The Cancer Stem Cell Hypothesismentioning

confidence: 92%

Breast Tumor Heterogeneity: Cancer Stem Cells or Clonal Evolution?

Campbell

Polyák²

2007

Cell Cycle

365

272

View full text Add to dashboard Cite

show abstract

“…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

View full text Add to dashboard Cite

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.

show abstract

“…Although some organisms use glycolysis preferentially during periods of sustained growth (because the byproducts are useful as building blocks in the anabolic process), glycolysis is highly inefficient when oxygen is not a limiting factor because the anaerobic metabolism of glucose to lactic acid produces fewer ATP molecules per molecule of glucose than oxidation to CO 2 and H 2 O, and therefore leads to slower proliferation. Since cancer progression is a process of clonal selection (Cairns, 1975;Nowell, 1976;Crespi and Summers, 2005;Merlo et al, 2006;Greaves and Maley, 2012), upregulation of glycolysis must confer a selective advantage to a cell to compensate for its slower proliferation. If it is not simply an adaptation to hypoxia, what is the adaptive value of the Warburg effect for cancer cells?…”

Section: The Warburg Effectmentioning

confidence: 99%

Evolutionary dynamics of the Warburg effect: Glycolysis as a collective action problem among cancer cells

Archetti

2014

Journal of Theoretical Biology

View full text Add to dashboard Cite

The upregulation of glycolysis in tumors is common even when oxygen is not limiting. The adaptive value of this "Warburg effect" is unclear. Glycolysis is costly for a cell but the ensuing acidity is beneficial for the tumor. A collective action problem among cancer cells arises. Game theory shows that the acidity induced by glycolysis can explain the Warburg effect. a r t i c l e i n f o a b s t r a c tThe upregulation of glycolysis in cancer cells (the "Warburg effect") is common and has implications for prognosis and treatment. As it is energetically inefficient under adequate oxygen supply, its adaptive value for a tumor remains unclear. It has been suggested that the acidity produced by glycolysis is beneficial for cancer cells because it promotes proliferation against normal cells. Current models of this acid-mediated tumor invasion hypothesis, however, do not account for increased glycolysis under nonlimiting oxygen concentrations and therefore do not fully explain the Warburg effect. Here I show that the Warburg effect can be explained as a form of cooperation among cancer cells, in which the products of glycolysis act as a public good, even when oxygen supply is high enough to make glycolysis energetically inefficient. A multiplayer game with non-linear, non-monotonic payoff functions that models the benefits of the acidity induced by glycolysis reveals that clonal selection can stabilize glycolysis even when energetically costly, that is, under non-limiting oxygen concentration. Characterizing the evolutionary dynamics of glycolysis reveals cases in which anti-cancer therapies that rely on the modification of acidity can be effective.

show abstract

Evolutionary biology of cancer

Cited by 232 publications

References 80 publications

Breast Tumor Heterogeneity: Cancer Stem Cells or Clonal Evolution?

Breast Tumor Heterogeneity: Cancer Stem Cells or Clonal Evolution?

Cooperation among cancer cells as public goods games on Voronoi networks

Evolutionary dynamics of the Warburg effect: Glycolysis as a collective action problem among cancer cells

Contact Info

Product

Resources

About