Abstract
We present a mathematical model that captures the transitions among three experimentally observed estrogen-sensitivity phenotypes in breast cancer cells. Based on this model, a population-level model is created and used to explore the optimization of a therapeutic protocol
Footnotes
Research supported by the National Cancer Institute. The authors are with the Virginia Polytechnic Institute and State University, Blacksburg, VA. (email: last_name{at}vt.edu).
Copyright
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