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Treachery of immune cells promotes deadly cancer : Study
Washington, Aug 18 (IANS):
Published on 18 Aug. 2009 11:42 PM IST
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Immune cells or macrophages that protect us against invaders or disease, turn traitors and actually help some of the deadliest cancers to progress, says a new study. Albert Einstein College cancer researcher Jeffrey W. Pollard and seven colleagues analysed the movement of breast cancer cells in mice to show that a distinct population of macrophages helps malignant cells set up shop at distant sites. This process, known as metastasis, is the main reason cancer patients die. Pollard and his colleagues believe that their discovery offers a potentially useful new target for anti-cancer therapy. What they’ve found is a vulnerable step in the cancer process that might be blocked by drug treatments. In three different ways, the scientists showed that metastatic tumour growth is inhibited if these unusual macrophages are killed. They also showed that even after breast cancer cells have lodged in the animals’ lungs and started aggressive growth, erasing the special macrophages dramatically slowed growth of the metastasized tumors. “This suggests that anti-macrophage therapy will have an impact in patients even with metastatic disease,” Pollard said. Based on this new work, he added: “Macrophages themselves, or their unique signalling pathways, represent new therapeutic targets that may be efficacious in reducing cancer mortality.” Ordinarily, macrophages are vital for maintaining health as an integral arm of the immune system, one of the body’s main lines of defence. Their assigned tasks include cleaning up debris in the wake of disease or injury, alerting other immune system cells when an infection begins, and helping identify viruses and bacteria that need to be killed, said an Einstein release. “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,” Pollard explained. The new study was published online in PLoS ONE

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