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Tumor-Associated Macrophages: From Mechanisms to Therapy
The tumor microenvironment is a complex ecology of cells that evolves with and provides support to tumor cells during the transition to malignancy. Among the innate and adaptive immune cells recruited to the tumor site, macrophages are particularly abundant and are present at all stages of tumor pro...
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Published in: | Immunity (Cambridge, Mass.) Mass.), 2014-07, Vol.41 (1), p.49-61 |
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Main Authors: | , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | The tumor microenvironment is a complex ecology of cells that evolves with and provides support to tumor cells during the transition to malignancy. Among the innate and adaptive immune cells recruited to the tumor site, macrophages are particularly abundant and are present at all stages of tumor progression. Clinical studies and experimental mouse models indicate that these macrophages generally play a protumoral role. In the primary tumor, macrophages can stimulate angiogenesis and enhance tumor cell invasion, motility, and intravasation. During monocytes and/or metastasis, macrophages prime the premetastatic site and promote tumor cell extravasation, survival, and persistent growth. Macrophages are also immunosuppressive, preventing tumor cell attack by natural killer and T cells during tumor progression and after recovery from chemo- or immunotherapy. Therapeutic success in targeting these protumoral roles in preclinical models and in early clinical trials suggests that macrophages are attractive targets as part of combination therapy in cancer treatment.
Macrophages promote tumor progression to malignancy. Noy and Pollard discuss how macrophages both stimulate tumor cell growth and suppress antitumor immune responses and propose ablation or redifferentiation of macrophages in tumors as a promising therapeutic approach to treat cancer. |
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ISSN: | 1074-7613 1097-4180 |
DOI: | 10.1016/j.immuni.2014.06.010 |