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      Tumor-associated macrophages: from mechanisms to therapy.

      1 , 2
      Immunity
      Elsevier BV

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          Abstract

          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.

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          Author and article information

          Journal
          Immunity
          Immunity
          Elsevier BV
          1097-4180
          1074-7613
          Jul 17 2014
          : 41
          : 1
          Affiliations
          [1 ] Department of Developmental and Molecular Biology, Center for the Study of Reproductive Biology and Women's Health, Albert Einstein College of Medicine, New York, NY 10461, USA.
          [2 ] Department of Developmental and Molecular Biology, Center for the Study of Reproductive Biology and Women's Health, Albert Einstein College of Medicine, New York, NY 10461, USA; MRC Centre for Reproductive Health, Queen's Medical Research Institute, The University of Edinburgh, Edinburgh EH16 4TJ, UK. Electronic address: jeff.pollard@ed.ac.uk.
          Article
          S1074-7613(14)00230-1 NIHMS611895
          10.1016/j.immuni.2014.06.010
          4137410
          25035953
          b2f5345b-47ef-4ad2-8c9b-35ee83314587
          Copyright © 2014 Elsevier Inc. All rights reserved.
          History

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