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Tumor-Associated Macrophages: From Basic Research to Clinical Application

A special issue of Journal of Clinical Medicine (ISSN 2077-0383). This special issue belongs to the section "Oncology".

Deadline for manuscript submissions: closed (1 May 2021) | Viewed by 3796

Special Issue Editor


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Guest Editor
Institute of Transfusion Medicine and Immunology, Mannheim Institute for Innate Immunoscience (MI3), Medical Faculty Mannheim, Heidelberg University, 68167 Mannheim, Germany
Interests: transcriptional, epigenetic, and metabolic programming of macrophages and their precoursors—corculating monocytes; tumor immunometabolism; macrophage biomarkers of therapy resistance; new molecular targets for TAM reprogramming in solid tumors
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Special Issue Information

Dear Colleagues,

Tumor-associated macrophages (TAMs) are major innate immune cells in a tumor microenvironment and can constitute up to 50% of the mass of human tumors. TAMs are highly heterogeneous cells that originate from resident tissue-specific macrophages and from newly recruited monocytes. TAM variability strongly depends on cancer type, stage, and intratumoral heterogeneity. The majority of TAMs are programmed by TME to support primary tumor growth and metastatic spread. However, in some types of cancer, TAM can also restrict tumor growth and metastasis. TAM can also cooperate or interfere with anticancer therapy. There are three major mechanistic levels that define macrophages phenotype and functional polarization: transcriptional factors, epigenetic modifications, and metabolic pathways, and understanding the complexity of the interaction between thee pathways is the next challenge that will allow identifying pharmacological targets for immunomodulatory therapy in specific tumor types. The development of delivery systems for specific targeting for pro-tumoral TAMs in different types of cancer is the next task for biotechnology.

In the Special Issue, we invite submissions that describe fundamental aspects of TAM biology, interaction of TAM with cancer cells, and other cells in tumor microenvironment; novel preclinical models to decipher the function of TAM; association of TAM with various human cancers; new TAM biomarkers for the prediction of metastasis and therapy responses; therapeutic targets in TAM, and immunomodulatory therapeutic approaches based on targeting of TAM. 

Prof. Dr. Julia Kzhyshkowska
Guest Editor

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Keywords

  • tumor-associated macrophage
  • cytokine
  • transcriptional program
  • signal transduction
  • epigenetics
  • phagocytosis
  • biomarker
  • cancer
  • metastasis
  • immunotherapy

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Published Papers (1 paper)

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Review

11 pages, 1270 KiB  
Review
Challenges and Opportunities for Immunotherapeutic Intervention against Myeloid Immunosuppression in Glioblastoma
by Mark A. Exley, Samantha Garcia, Amelia Zellander, Jenny Zilberberg and David W. Andrews
J. Clin. Med. 2022, 11(4), 1069; https://doi.org/10.3390/jcm11041069 - 18 Feb 2022
Cited by 6 | Viewed by 3347
Abstract
Glioblastoma multiforme (GBM), the most common and deadly brain cancer, exemplifies the paradigm that cancers grow with help from an immunosuppressive tumor microenvironment (TME). In general, TME includes a large contribution from various myeloid lineage-derived cell types, including (in the brain) altered pathogenic [...] Read more.
Glioblastoma multiforme (GBM), the most common and deadly brain cancer, exemplifies the paradigm that cancers grow with help from an immunosuppressive tumor microenvironment (TME). In general, TME includes a large contribution from various myeloid lineage-derived cell types, including (in the brain) altered pathogenic microglia as well as monocyte-macrophages (Macs), myeloid-derived suppressor cells (MDSC) and dendritic cell (DC) populations. Each can have protective roles, but has, by definition, been coopted by the tumor in patients with progressive disease. However, evidence demonstrates that myeloid immunosuppressive activities can be reversed in different ways, leading to enthusiasm for this therapeutic approach, both alone and in combination with potentially synergistic immunotherapeutic and other strategies. Here, we review the current understanding of myeloid cell immunosuppression of anti-tumor responses as well as potential targets, challenges, and developing means to reverse immunosuppression with various therapeutics and their status. Targets include myeloid cell colony stimulating factors (CSFs), insulin-like growth factor 1 (IGF1), several cytokines and chemokines, as well as CD40 activation and COX2 inhibition. Approaches in clinical development include antibodies, antisense RNA-based drugs, cell-based combinations, polarizing cytokines, and utilizing Macs as a platform for Chimeric Antigen Receptors (CAR)-based tumor targeting, like with CAR-T cells. To date, promising clinical results have been reported with several of these approaches. Full article
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