We recently identified a vicious cycle between granulocyte macrophage colony stimulating factor (GM-CSF) arising from breast cancer cells that have undergone epithelial-mesenchymal transition (EMT) and the tumor-associated macrophage (TAM)-derived chemokine CCL18, a signaling loop that promotes tumor metastasis. Tumor-derived lactate skews GM-CSF-activated macrophages to an anti-inflammatory and immunosuppressive M2 phenotype, suggesting that breaking this cycle in combination with glycolysis inhibitors may inhibit tumor development.
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Su et al. (2014) studied this question.
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