Tumor-associated macrophages in thoracic malignancies

Our plain-English summary of Tumor-associated macrophages in thoracic malignancies, by L.A. Lievense, K. Bezemer, J.G. Aerts, et al (Lung Cancer, 2013).

The study

• Authors: L.A. Lievense, K. Bezemer, J.G. Aerts, J.P. Hegmans
• Journal: Lung Cancer
• Published: 2013;80(3):256-62
• Type of article: Review
• Cited by: 50 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

Abstract

Tumor-associated macrophages (TAMs) can be abundantly present in numerous cancer types. Under influence of various stimuli in the tumor microenvironment TAMs develop into a tumor-inhibitory (M1) or tumor-promoting (M2) phenotype. Recently, the role of TAMs in tumor biology and their prognostic value in cancer has become a major topic of interest. In this review we will discuss the importance of TAMs in the pathogenesis and clinical outcome of lung cancer and mesothelioma patients. In addition, the potential of TAMs as therapeutic targets will be discussed.

Copyright © 2013 Elsevier Ireland Ltd. All rights reserved.

In plain English

This article was a review, not a new study. The authors discussed published research on tumor-associated macrophages (TAMs), a type of immune cell found in tumors, in non-small cell lung cancer and malignant mesothelioma, and on possible treatments aimed at these cells. The authors noted that mesothelioma is strongly associated with exposure to airborne asbestos fibers. They described a process in which macrophages that cannot clear asbestos fibers cause chronic inflammation. Among the work reviewed, a study by Burt et al. of 667 pleural mesothelioma patients who underwent cytoreduction between 1989 and 2009 reported that higher TAM densities were associated with poor survival in nonepithelial mesothelioma. The authors' own group had reported that removing macrophages with clodronate inhibited tumor growth in a mouse mesothelioma model. For non-small cell lung cancer, studies of macrophages and prognosis had given contradictory results. The authors wrote that, unlike in non-small cell lung cancer, little was known about the type and function of macrophages in mesothelioma, and that no clinical drugs specifically targeted TAMs. The authors concluded that targeting TAMs may improve cancer treatment.

We wrote this plain-English summary from the full article with the help of AI, and a second AI model checked each sentence against the article. It is not the authors' wording; the abstract and the article are their own account.

What the study did and found

• Design: Narrative review of published research
• Who was studied: No new population was studied. The review covered published research on tumor-associated macrophages in non-small cell lung cancer and malignant mesothelioma, including human, laboratory and mouse studies.
• Exposure: Not an exposure study. As background, the authors stated that mesothelioma is strongly associated with exposure to airborne asbestos fibers (no fiber type named). They described macrophages failing to clear the fibers, leading to chronic inflammation.
• Main results:
  • Reviewed study (Burt et al.), not this article's own data: it examined circulating monocytes and TAMs in 667 pleural mesothelioma patients who underwent cytoreduction between 1989 and 2009.
  • Same reviewed study (Burt et al.): in these patients, higher numbers of circulating monocytes were associated with poor survival.
  • Same reviewed study (Burt et al.): in patients with nonepithelial mesothelioma, higher densities of TAMs were associated with poor survival.
  • Earlier work by the authors' group in a mouse mesothelioma model: depleting macrophages with clodronate inhibited tumor growth.
  • Earlier work by the authors' group in the mouse mesothelioma model: zoledronic acid reduced TAMs, but survival did not improve.
  • Reviewed study (Welsh et al.) in non-small cell lung cancer: macrophages inside tumor islets were related to a good prognosis, while macrophages in the tumor stroma were related to a bad prognosis.
  • The authors described asbestos fibers that macrophages cannot eliminate as causing a chronic state of inflammation, which they linked to the development of mesothelioma.
  • The authors reported that no clinical agents were available that specifically target TAMs.
• The authors' conclusion: The authors concluded that characterizing TAM subtypes has proven challenging, and that targeting TAMs may improve treatment of non-small cell lung cancer and malignant mesothelioma by changing the tumor-protective environment.
• Limitations the authors state:
  • The authors stated that, unlike in non-small cell lung cancer, little was known about the phenotype and function of macrophages in malignant mesothelioma.
  • The authors stated that studies of macrophages and prognosis in non-small cell lung cancer had given contradictory results.
  • The authors stated that, to their knowledge, there were no clinical studies on the role of TAMs in small cell lung cancer.

Topics

The National Library of Medicine indexes this study under subjects our site covers: Lung cancer, Mesothelioma.

Medical terms in this study, explained in our Lexicon: Macrophage, Tumor Microenvironment, Lung Cancer, Mesothelioma.

Related studies

• Intratumoral macrophage phenotype and CD8+ T lymphocytes as potential tools to predict local tumor outgrowth at the intervention site in malignant pleural mesothelioma — R. Cornelissen, L.A. Lievense, et al. (2015)
• Pleural Effusion of Patients with Malignant Mesothelioma Induces Macrophage-Mediated T Cell Suppression — L.A. Lievense, R. Cornelissen, et al. (2016)
• Precision immunotherapy; dynamics in the cellular profile of pleural effusions in malignant mesothelioma patients — L.A. Lievense, K. Bezemer, et al. (2017)
• Antibody drug conjugates in thoracic malignancies — J.M. Pacheco, D.R. Camidge (2018)
• Tumor-associated macrophage-derived inflammatory cytokine enhances malignant potential of malignant pleural mesothelioma — D. Horio, T. Minami, et al. (2020)
• Depletion of Tumor-Associated Macrophages with a CSF-1R Kinase Inhibitor Enhances Antitumor Immunity and Survival Induced by DC Immunotherapy — F. Dammeijer, L.A. Lievense, et al. (2017)

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