A relatively complex model of prostate cancer to bone metastases

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CancerEvo got some good news last week. The paper that we have been working together with the Lynch Lab has now been accepted for publication at Cancer Research. Of course being accepted and being published are two different things so it might take a few weeks before those of you with the right subscription get access to the research but we are working to get something in biorxiv in the next few days.

Expect to find a relatively complex model based on the hybrid discrete continuum CA paradigm. That is, an agent based model where cells are governed by rules and molecules like TGF-Beta and RANKL are described by partial differential equations (PDEs).

Did I mention that this model is relatively complex? Well, it kind of is and it is no accident. In general mathematical oncologists pride themselves in producing the simplest mathematical models that fit the problem: the simplest most elegant model is always the best. But I am not sure whether this approach works so well when studying things like homeostasis. Homeostasis in the bone emerges from the interactions of a variety of cells like osteoclasts, osteoblasts, MSCs, etc. Successful metastases to the bone will have to disrupt this homeostasis and co-opt these interactions for their own advantage.

Some of these are mediated by molecules like TGF-Beta and RANKL and that is what we have investigated in this work but I also wonder whether we are missing out by just restricting ourselves to the molecules and cell types that have been the focus of attention by experimentalists. Of course the advantage of doing that is that we have a solid understanding of the known biology thanks to Leah Cook and Conor Lynch.

Which leads me to another point: usually mathematical oncologist work with experimentalist at specific points of the development of a project. Hopefully at inception (not always), then later on when there’s some model results to discuss and finally during the writing of the manuscript. Conor and Leah were involved at every step of this project, which I think is one of the reasons why we could get away with a little bit of extra complexity in this case. It is unfortunate that the current academic publishing system still does not have a way to acknowledge authors in projects with more than one PI and more than one postdoc doing the bulk of the work. At least you, the reader of this post, knows.

2 thoughts on “A relatively complex model of prostate cancer to bone metastases

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