Tumors Require Help from Macrophages to Metastasize

Cancer researchers have found that metastasis relies on the cooperation of a distinct sub-population of macrophages, a link that may be broken by appropriate drug intervention.

Investigators at the Albert Einstein College of Medicine (New York, NY, USA) analyzed the movement of breast cancer cells in mice. They reported in the August 10, 2009, online edition of the journal PLoS ONE that a population of host macrophages displaying a distinct phenotype was recruited by roaming pulmonary metastatic cells regardless of species of origin.

Reduction of this macrophage population through three independent means (genetic and chemical) showed that these macrophages were required for efficient metastatic seeding and growth. Importantly, even after metastatic growth was established, elimination of this macrophage population inhibited subsequent growth.

"This new study is important because it definitively shows the effects of macrophages at distant sites, as well as the identity of the macrophage population," explained senior author Dr. Jeffrey W. Pollard, professor of developmental and molecular biology at Albert Einstein College of Medicine. "This is the first proof that they have impact at this location, at the site of metastatic tumor growth."

"This suggests that antimacrophage therapy will have an impact in patients even with metastatic disease," said Dr. Pollard. "Macrophages themselves, or their unique signaling pathways, represent new therapeutic targets that may be efficacious in reducing cancer mortality."

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