A literature-parameterized ODE model of five TNBC cell populations ranks tumor proliferation, CAF-driven growth support, and M2-macrophage support as the biggest drivers of Day-168 tumor burden.
Cancer-associated fibroblasts induce epithelial–mesenchymal transition of breast cancer cells through paracrine TGF- β signalling
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Identifying Therapeutic Targets for Triple-Negative Breast Cancer using a Novel Mathematical Model of the Tumor Microenvironment
A literature-parameterized ODE model of five TNBC cell populations ranks tumor proliferation, CAF-driven growth support, and M2-macrophage support as the biggest drivers of Day-168 tumor burden.