Linda A. Snyder

TL;DR: The mechanistic link between CCL2 expression and macrophage infiltration are correlated with poor prognosis and metastatic disease in human breast cancer and the origin of these macrophages is defined by showing that Gr1-positive inflammatory monocytes are preferentially recruited to pulmonary metastases but not to primary mammary tumours in mice.

TL;DR: It is demonstrated that carcinoma-associated fibroblasts (CAF) are major sources of chemokines that recruit granulocytes to tumors, and CSF1R inhibitor with a CXCR2 antagonist blocked granulocyte infiltration of tumors and showed strong anti-tumor effects.

TL;DR: It is shown that treatment with anti-CCL2/JE antibody attenuated PC-3Luc-mediated overall tumor burden in the authors' in vivo model of prostate cancer metastasis by 96% at 5 weeks postintracardiac injection, and an interaction between tumor-derived chemokines and host-derived Chemokines acting in cooperation to promote tumor cell survival, proliferation, and metastasis is suggested.

TL;DR: The data suggest that CCL2 contributes to prostate cancer growth through the regulation of macrophage infiltration and enhanced angiogenesis within the tumor.

TL;DR: Administration of anti-CCL2/CCL12 antibodies along with the vaccines markedly augmented efficacy with enhanced reduction in tumor volume and cures of approximately half of the tumors, suggesting that combining CCL2 neutralization with vaccines should be considered in future immunotherapy trials.