Interview with mathematical biologist Luigi Preziosi

I guess it will be irrelevant for those of you that don’t speak Spanish but the Spanish news paper El Pais has interviewed the mathematical biologist Luigi Preziosi. Luigi happens to be one of the coordinators of the EU Marie Curie Network in which I am involved.

In the interview he argues that biology is geting more mathematical, explains how mathematicians and life scientists and physicians collaborate, how the mathematical models can help to explain medical phenomena and hint to innovative therapies. He also says that traditional biologists are still necessary (as if that was not obvious: theoretical physicists still need experimentalist to work with so they can validate their theories, it should not be different in the life sciences, there would not be biology without people that know how to perform experiments).

Bach et al: An evolutionary-game model of tumour-cell interactions

L.A. Bach, S.M. Bentzen, J. Alsner and F.B. Christiansen. An evolutionary-game model of tumour-cell interactions: possible relevance to gene therapy. European Journal of Cancer 27 (2001) 2116-2120.

Bach et al have taken the work from Tomlinson and Bodmer (which I reviewed a few day ago) in which angiogenesis is studied with the help a Game Theory. In the previous case the game involved two players who could chose to produce angiogenic factors or to do nothing. As long as one of the players is willing to shoulder on the cost of producing the factor, both players get the benefit. As expected the result is a polymorphism in which both types of strategies coexist. I said that this polymorphism is to be expected since if there were only factor producing cells then non cooperating cells will have an advantage (since they get the benefits without paying the costs) whereas if the population is made of non cooperating cells then factor producing cells will have an advantage (as long as the benefit of producing the factor is higher than the cost).

The revision of the model proposed by Bach et al considers the implications of extending the game to three players if the benefits of angiogenesis appear only if two out of the three players cooperate to produce the factor.

The payoff table would look like this:

A+,A+ A+,A- A-, A-
A+ 1-i+j 1-i+j 1-i
A- 1+j 1+j 1

where A+ means factor producing and A- means that is not factor producing. Also i is the cost of producing the factor and j is the benefit.

Bach et al analyse how these cost and benefit parameters affect the equilibria and the existence of polymorphism. For this they use computer simulations and find that when the benefit is three times the cost something interesting happens. In that case the final composition of the tumour population would be a consequence of the composition of the original population. Most likely this finding has limited (if any) consequences in potential therapies since physicians have not got the ability to change the initial composition of phenotypes in a tumour. Still, the (qualitative) results can be used as a guide for gene therapies.

Tumour supressor gene involved in virus protection

Got this from mainstream media but the paper itself has been published in the EMBO journal in September. Researchers at the Madrid based Centre for Oncological Research have found a gene (for those interested in the gene itself: ARF) that is implicated in both tumour supression and protection from viral infection.

I guess this amounts to another cellular mechanism that has been successfully evolved to adopt an extra new function. The results of evolution can be messy but I’m still impressed.

Darwin online


Heard it on the radio this morning while listening to the BBC: the University of Cambridge has digitised the text and images of thousands of pages from the publications of Charles Darwin. The website can be found here: http://darwin-online.org.uk/.

Included in the collection are works on other members of the Darwin family (such as the almost-as-famous-as-his-grandson Erasmus Darwin) as well as mp3 audio books for those who would like something more intellectual to entertain their daily jog or gym workout.

Evolution and cancer news

Every morning I check a couple of sites in order to get an overview of what is going on in the world. Today I found a couple of curious things:

On the more serious (and cancer related) front, A group of researchers at the University of Missouri-Columbia have found a way to find out the spread of skin cancer cells through the blood. The technique relies on the fact that the vibrations produced by a laser into a melanoma cell is different from that of other cells like red blood cells and plasma.

More information can be obtained here (for those with a subscription to the journal of optics letters).
A different kind of research has been noticed by the bigger media (BBC, Telegraph) and it seems to illustrate how not to use the theory of evolution. Researchers at the Darwin centre at the London School of Economics have seen the future and came back to tell us: Mankind will split into two separate species: the clever and beautiful and the dim-witted goblin-like. I have already heard people labelling these groups as the Macs and the PCs.

Turning on genes again

I confess to read The Economist newspaper more than occasionally and I find the Science and Technology section readable but rigorous.In this week’s issue there is an article about a new class of drugs that has recently gained approval in the US.

One of the things I have learned reading this article is about how mutations might occur that could lead to tumour formation. Up to now, as far as I was concerned, a mutation is a mutation is a mutation, that is, something that just happens and, ooops, one more ticket for the lottery of cancer. Well, it seems that a curious way to turn off large parts of the DNA is by increasing the packing density of the DNA so it becomes effectively unreadable. It seems that cancer cells can use this mechanism to avoid expressing genes so they can proliferate faster as well as avoid apoptosis and senescence. Given that the drug that has just been granted regulatory approval works best with leukemia it seems that the mechanisms employed by tumour cells to deactivate certain cell mechanisms varies from cancer to cancer. Still, having cancer cells with the capability of turning off significant parts of the DNA is such an evolutionary advantage that it should not be surprising if equivalent mechanisms are found in other types of cancer.