remains an interesting open question, and answering it will require integrating the theories of sensing and communication with the models of collective migration described herein. For tumor cells in particular, an integrated physical theory of sensing and migration would prove immensely useful for identifying the key determinants of invasive capabilities. Identifying these determinants would help pinpoint the ways that these capabilities could be disrupted, using drugs and other therapies, as described next.

Drug sensitivity and implications for therapy
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We have seen that cells, including tumor cells, are remarkably precise sensors of molecules in their environment. This raises the question of how sensitive tumor cells are to drug molecules in their environment. What is the minimum drug concentration required not just for precise detection by a cell, but for causing a phenotypic change, such as cell death?

Experiments have shown that cancer cells are sensitive to very small drug concentrations. For example, lung carcinoma cells were exposed *in vitro* to various concentrations of the anti-cancer drug paclitaxel, also known as taxol, which acts to block mitosis in order to achieve cell death by disrupting microtubule regulation [@torres1998mechanisms]. Paclitaxel concentrations as low as $1$ nM were shown to affect microtubule dynamics 