CCL2 and pleural neoplasm: Equally importantly, the data strengthen the above mechanistic views on MPE pathobiology: in our hands anti-CCL2/12 effects were not restricted to inhibiting tumor growth, but included blunting of emergent tumor-to-host signaling events resulting in reduced recruitment of inflammatory cells to the malignancy-affected pleura, disruption of pleural tumor vasculature, and down-regulated permeability of juxtapleural blood vessels.