Based at the Moffitt Cancer Center, Florida, Cancer Ecology is a small research group led by David Basanta. We are mathematical modellers who work with biologists and clinicians, trying to understand the ecology of tumors and the evolutionary dynamics of cancer progression and resistance to treatment.

Mistakes and evolution

I do follow some scienceblogs out there. The New York Times hosts one from Olivia Judson called The Wild Side about evolutionary biology. The blog is very well written, which is not surprise coming from a professional writer (and research fellow at Imperial College London). The entry a few days ago was about the role of mistakes in evolution. The mistakes she was writing about are the mutations that occur duplicating the genetic material during cell division.

What she argues is that mutations are not necessarily an imperfection of our reproductive system but, especially in asexual species, the means for adaptation. The claim gets more interesting because, if a given rate of mutations is something that allows adaptation, then the mutation rate itself could be subject to adaptation. Turns out that this is true. As I had read before somewhere else and as I blogged about before when talking about the mutator phenotype hypothesis, the mutation rate adapts itself in order to suit the particular environment in which the evolving system lives (I’d rather call it evolving system since RNA viruses are not normally considered living beings). Thus in difficult environments it pays off to have a higher rate of mutation so that a viable phenotype will be found quickly even at the cost of having to produce plenty of absolutely inviable phenotypes at the same time. In nicer environments where many alternative phenotypes can survive then, a high mutation rate is more likely to be counter productive.

These facts should be applicable to cancer. The rate of mutation can be altered by changes in the DNA repair machinery and the various checkpoints in the cell cycle. Some cells with perfectly functioning DNA repair mechanisms are unlikely to divide producing mutations along the way. Others with mutations in, say, p53, are more likely to make mistakes during mitosis. As a consequence, someone correct me if I am wrong here, it should be reasonable to expect that tumour cells in those parts of a tumour that inhabit harsh micro-environments, should have a higher rate of mutation. This higher rate of mutation should be the result not only of the fact that tumour cells keep accumulating genetic aberrations but more importantly, from the fact that those cells in harsh environments that insist in keeping a well oiled and preserved division mechanism will be less likely to adapt and survive. Seems like an interesting problem that could be formulated in terms of mathematical biology.

Evolution and drug resistance

Science in Spain