One of the things I had in mind when I started this blog is that I could use it to force me to write reviews about some of the most relevant papers that I often read for my own ‘dirty’ purposes. Usual reasons apply: it is good to write about what you read since synthesis helps understanding.
In any case, as you know, one of the topics I am interested on is cancer research using evolutionary game theory and although evolution is not what these people have studied the other important keywords are present in this paper.
Mansury et al have devised a nice spatial (2D lattice) agent based (Cellular Automata style) system in which tumour cells inhabit a space with nutrients. Tumour cells can be found in two varieties: A (proliferative) and B (migratory). Non evolutionary game theory is used to analyse the interactions between cells that have different phenotypes and how those interactions reflect on the payoffs of the individual cells and on the tumour as a whole. The payoffs in this game are slightly more complicated (and according to the authors, more realistic) than those of other games. The payoff of a cells is made of three different factors: communication payoff, proliferation payoff and migration payoff.
For the simulations (since it is quite difficult to come with a nice analytical study) they run CAs with 500×500 lattices in which nutrients are diffused from the centre and the middle. From here they study how changing the payoff table results in different velocity of tumour growth, different tumour surface roughness (useful to analyse the malignancy of a tumour) and the numbers of both tumour populations with time
From my point of view, the most significant shortcoming of an otherwise interesting piece of research (and acknowledged by the authors) is the lack of evolution in the model. With evolution out of the equation the condition under which phenotypes emerge and take over the original population cannot be studied. One of the nice features of game theory is that it can be used to study the equilibrium states of tumour cell populations when those tumours are studied as composed of individual cells (or agents in Mansury’s et al model). Since the author’s know this I am looking forward their next paper to see how the improved model can be used to study carcinogenesis.