Harvard Medical School
We report three studies which use a combination of mathematical and experimental methods to study the process of cancer invasion. During invasion the proteolytic degradation of extracellular matrix proteins generates fragments which are chemotactically active. Using a model we investigated the consequnces of these chemotactic wakes. We then experimentally evaluted the prediction of the model. Together these studies showed that extracellular matrix mediated chemotaxis functions predominantly to impede invasion rather than encourage it. We also show that maximal migration requires an optimal match of adhesion and chemotaxis and consequently decreased cell migration can result from increasing chemotaxis. Lastly, we show that extracellular matrix concentration exerts selection pressure on invading cells.
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