Dr. Arturo Araujo

Congratulations to one of our members, Arturo Araujo on switching his Mr. to Dr. having successfully defended his PhD thesis at University College London last week.

 

Here we can see +Arturo Araujo celebrating with his PhD supervisor +Peter Bentley and his examiners +Alex Fletcher and +Philip Gerlee 

Exploiting ecological principles to better understand cancer progression and treatment

I talked about this before in Google+ but the paper +Alexander Anderson and myself authored at the Royal Society Interface focus is now available for everybody to see. This is a somewhat unconventional type of paper as it is not exactly a research paper, a review paper or an opinion piece but a combination of all those. I must apologise that the article is not in an open access journal but the version in arXiv has all the content (even if it's not as pretty as the journal version). Also, at least for some time, the article can be downloaded from Interface Focus [PDF].

By the way, the visuals of the article, including the following sketch by +Arturo Araujo describing the ecosystem of prostate cancer metastasis to bone, are quite impressive I think.

More on game theory and the evolution of invasive phenotypes

+Artem Kaznatcheev , a colleague at McGill University, has taken an old paper of ours and decided to do further analysis on it. The emergence of invasiveness is one of the hallmarks of cancer progression and space is likely to play a very important role. For that reason, I used both standard evolutionary game theory and cellular automata to see how much our original results would change if space is explicitly considered. The results can be found here. Now +Artem Kaznatcheev has worked on a Ohtsuki-Nowak transform so that we could still try to understand the role of space without sacrificing the analytical power of game theory. He blogged about it here and the preliminary results look promising. The number of neighbours a tumour cell has impacts the likelihood of motility to emerge in a tumour population. Hope we can learn more about this technique in the next few days now that +Artem Kaznatcheev is in Florida.

Back to blogger

I am back to blogger! Or to be more precise, we are. When I left blogger  a few years ago the idea was to start using a blogging platform that would allow me to share my ideas with likeminded people. That initially was Nature Networks, and eventually Google+. Now we are starting another experiment with blogger, one in which this blog will capture all the news and events related to the CancerEvo group at the Integrated Mathematical Oncology department at the H. Lee Moffitt Cancer Center in Tampa. Hope to see you all very often around these pages!

David and the CancerEvo group.

Moving to Nature Networks

Dear everybody.

From now on this blog is moving to Nature Networks. Find it following this link.

See you there!

Mini workshop in Oxford

Today Marcus Tindall has organised a mini symposium (for lack of a better name) for me and the guys here working on mathematical models of cancer to get to know each other. I have given a very small presentation [PDF] (<30m) that covers stuff I presented before.

From the CMB I got to know the work of:

• Philip Murray, who has created a CA model to study the role of the cell cycle in tumours and that is now trying to obtain a continuous model that displays the same behaviour.
• Alex Fletcher who studies hypoxia in tumour development at the sub-cellular scale.
• Matt Johnston who works with W. Bodmer (whose game theory models have inspired my own work) to study the dynamics of cell populations in a colon crypt in colorectal cancer. His model shows how a homeostatic population could explode by slightly altering some of the paramers.
• Natasha Li who collaborates with Gatenby to study, using Cellular Automaton and continuous models, the role of glycolysis in tumour invasion and the influence of the stromal environment. This is specially relevant to me since it is one of my two main lines of work at the moment. She mention in her talk that glycolytic cells are especially sensitive to glucose deprivation.
  
• Rebecca Carter works on multiscale models of fluid and drug transportation in tumours.
• Marcus Tindall gave a brief introduction to his multiscale model of interaction between the cell cycle and cell density.

The presentations were all quite short but I hope to hear more from these people in the coming days.

Queerer than we can suppose

I found this video from a Richard Dawkins's talk in which he talks about the strangeness of science.

He talks that science is about truth but that our brain is evolved to cope with every day's reality, within the scope of the reality we have to live with. He cites the example that matter is mostly composed of space but we do not perceive it like that since it is more useful for us to perceive it as solid and opaque. He argues that a living being of the size of a neutrino and capable of vision would see matter as mostly empty space only by the nature of the space it inhabits. Similarly, things that look entirely unlikely to us (the existence of life) become inevitable when considering the vast amounts of time and space the universe has been going on compared to the space and time of our human lifetimes.

More shockingly to me he claims that humans are more akin to automata than to agents seeking what they consider positive things and avoiding negative things. The reason being that evolutionarily we rather model fellow humans as people with a purpose than as systems made of components whose design and integration we ignore.

In any case this is an important issue for scientists and philosophers of science: our brains have evolved for certain purposes and with certain biases and that should impose some limitations and constraints in what things we can understand and how we chose to interpret natural phenomena.

Oxford

I will be staying one month at the Centre for Mathematical Biology directed by Philip Maini at the University of Oxford. With a little of luck I will be able to meet people interested in mathematical discrete models of cancer evolution and angiogenesis.

In the Centre they have some interesting (and relevant) research lines like "individual and collective behaviour in ecology" and of course "cancer modelling". The Centre is pioneering (with Arizona's Gatenby and Oxford's Comlab Gavaghan) the idea that glycolytic acidity promotes invasion. Maybe this could be an opportunity to test my hypothesis that this invasion comes in waves.

Talk in Girona

I have been invited by Josep Vehi to give a talk about my research at the institute he directs at the University of Girona.

In this talk I have introduced for the first time the game theory model in which I have worked with people in Dresden (Andreas Deutsch, Haralambos Hatzikirou) and Bonn (Matthias Simon) in which I study Gatenby's hypothesis of acid mediated tumour invasion. I have also talked about the Cellular Automata model I have developed with Benjamin Ribba (Lyon) to study the microenvironmental influence in cancer evolution which I have previously presented in Lyon, Dundee and Dresden.

The presentation can be found here in PDF format.

cancer and the cell cycle

Last Friday I came to the Max Planck Instute for Cell Biology, at the other side of Dresden, to attend a series of seminars including one from a colleague and friend of mine, Babis Hatzikirou, about the cell cycle.

The classical view on the cell cycle can be seen in this picture that I took from Babis's presentation (and which I suspect he took from somewhere else :)):
This is quite interesting although not precisely research news. Most of the cell cycle is of course devoted to interphase and only a minority of the time (assuming that the cell is not in arrest mode) is devoted to create a copy of itself (through mitosis and cytokinesis). The cell cycle is controlled by a finely tuned balance of proteins cdc2-cdc13 and a number of checkpoints make sure that before changing the phase of the cell cycle everything is in order. These checkpoints and their associated proteins (such as the famous TP53) are quite critical to prevent tumour formation as they impede the growth of cells that need DNA repair.