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      Interaction of tumor-associated macrophages and cancer chemotherapy

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          ABSTRACT

          It has been recently recognized that the tumor microenvironment (TME) is an essential factor that defines the efficiency of chemotherapy. The local TME, consisting of immune cells with diverse phenotypes and functions, can strongly modulate the response to chemotherapy. Tumor-associated macrophages (TAMs) that display pronounced heterogeneity and phenotypic plasticity are the major innate immune component in the microenvironment of solid tumors. In our review, we elucidate the complex role of TAMs in the progression of different types of solid tumors, summarize the current knowledge about the effects of different anticancer chemotherapeutic agents on monocytes/macrophages, and describe the mechanisms of chemotherapy resistance mediated by TAMs.

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          Leukocyte complexity predicts breast cancer survival and functionally regulates response to chemotherapy.

          David G DeNardo, Donal J Brennan, Elton Rexhepaj … (2011)
          Immune-regulated pathways influence multiple aspects of cancer development. In this article we demonstrate that both macrophage abundance and T-cell abundance in breast cancer represent prognostic indicators for recurrence-free and overall survival. We provide evidence that response to chemotherapy is in part regulated by these leukocytes; cytotoxic therapies induce mammary epithelial cells to produce monocyte/macrophage recruitment factors, including colony stimulating factor 1 (CSF1) and interleukin-34, which together enhance CSF1 receptor (CSF1R)-dependent macrophage infiltration. Blockade of macrophage recruitment with CSF1R-signaling antagonists, in combination with paclitaxel, improved survival of mammary tumor-bearing mice by slowing primary tumor development and reducing pulmonary metastasis. These improved aspects of mammary carcinogenesis were accompanied by decreased vessel density and appearance of antitumor immune programs fostering tumor suppression in a CD8+ T-cell-dependent manner. These data provide a rationale for targeting macrophage recruitment/response pathways, notably CSF1R, in combination with cytotoxic therapy, and identification of a breast cancer population likely to benefit from this novel therapeutic approach. These findings reveal that response to chemotherapy is in part regulated by the tumor immune microenvironment and that common cytotoxic drugs induce neoplastic cells to produce monocyte/macrophage recruitment factors, which in turn enhance macrophage infiltration into mammary adenocarcinomas. Blockade of pathways mediating macrophage recruitment, in combination with chemotherapy, significantly decreases primary tumor progression, reduces metastasis, and improves survival by CD8+ T-cell-dependent mechanisms, thus indicating that the immune microenvironment of tumors can be reprogrammed to instead foster antitumor immunity and improve response to cytotoxic therapy.
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            Immunological aspects of cancer chemotherapy.

            Laurence Zitvogel, Lionel Apetoh, François Ghiringhelli … (2008)
            Accumulating evidence indicates that the innate and adaptive immune systems make a crucial contribution to the antitumour effects of conventional chemotherapy-based and radiotherapy-based cancer treatments. Moreover, the molecular and cellular bases of the immunogenicity of cell death that is induced by cytotoxic agents are being progressively unravelled, challenging the guidelines that currently govern the development of anticancer drugs. Here, we review the immunological aspects of conventional cancer treatments and propose that future successes in the fight against cancer will rely on the development and clinical application of combined chemo- and immunotherapies.
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              How Taxol/paclitaxel kills cancer cells

              Beth Weaver (2014)
              Taxol (generic name paclitaxel) is a microtubule-stabilizing drug that is approved by the Food and Drug Administration for the treatment of ovarian, breast, and lung cancer, as well as Kaposi's sarcoma. It is used off-label to treat gastroesophageal, endometrial, cervical, prostate, and head and neck cancers, in addition to sarcoma, lymphoma, and leukemia. Paclitaxel has long been recognized to induce mitotic arrest, which leads to cell death in a subset of the arrested population. However, recent evidence demonstrates that intratumoral concentrations of paclitaxel are too low to cause mitotic arrest and result in multipolar divisions instead. It is hoped that this insight can now be used to develop a biomarker to identify the ∼50% of patients that will benefit from paclitaxel therapy. Here I discuss the history of paclitaxel and our recently evolved understanding of its mechanism of action.
              Article 0 comments Cited 509 times – based on 0 reviews     Review now
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                Author and article information

                Journal
                Journal ID (nlm-ta): Oncoimmunology
                Journal ID (iso-abbrev): Oncoimmunology
                Journal ID (publisher-id): KONI
                Journal ID (publisher-id): koni20
                Title: Oncoimmunology
                Publisher: Taylor & Francis
                ISSN (Print): 2162-4011
                ISSN (Electronic): 2162-402X
                Publication date Collection: 2019
                Publication date (Electronic): 13 April 2019
                Publication date PMC-release: 13 April 2019
                Volume: 8
                Issue: 7
                Electronic Location Identifier: 1596004
                Affiliations
                [a ]Laboratory of Translational Cellular and Molecular Biomedicine, National Research Tomsk State University , Tomsk, Russia
                [b ]laboratory of molecular oncology and immunology, Cancer Research Institute, Tomsk National Research Medical Center, Russian Academy of Sciences , Tomsk, Russia
                [c ]Department of Innate Immunity and Tolerance, University of Heidelberg, Medical Faculty Mannheim, Institute of Transfusion Medicine and Immunology , Mannheim, Germany
                [d ]German Red Cross Blood Service Baden-Württemberg – Hessen , Mannheim, Germany
                Author notes
                CONTACT Julia Kzhyshkowska julia.kzhyshkowska@ 123456gmail.com Institute of Transfusion Medicine and Immunology, Medical Faculty Mannheim, Heidelberg University , Theodor-Kutzer Ufer 1-3, Mannheim D-68167
                Author information
                http://orcid.org/0000-0002-7206-8624
                Article
                Publisher ID: 1596004
                DOI: 10.1080/2162402X.2019.1596004
                PMC ID: 6527283
                PubMed ID: 31143517
                SO-VID: 46e37f7b-8d34-4872-b156-ac9946835182
                Copyright © © 2019 The Author(s). Published with license by Taylor & Francis Group, LLC.
                License:

                This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivatives License ( http://creativecommons.org/licenses/by-nc-nd/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited, and is not altered, transformed, or built upon in any way.

                History
                Date received : 24 December 2018
                Date revision received : 17 February 2019
                Date accepted : 9 March 2019
                Page count
                Figures: 2, Tables: 2, References: 121, Pages: 15
                Funding
                Funded by: Russian Science Foundation 10.13039/501100006769
                This work was supported by the Russian Science Foundation under Grand #14-15-00350. The PhD position of Tengfei Liu was supported by the program of China Scholarship Council No.201308130088.
                Categories
                Subject: Review

                ScienceOpen disciplines: Immunology
                Keywords: tumor-associated macrophages,cancer chemotherapy,chemoresistance,immunomodulation,tumor progression,immune system
                Data availability:
                ScienceOpen disciplines: Immunology
                Keywords: tumor-associated macrophages, cancer chemotherapy, chemoresistance, immunomodulation, tumor progression, immune system

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