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The Association Between Tumor-Associated Macrophages and Glioblastoma: A Potential Target for Therapy Publisher Pubmed



Heidari A1, 2 ; Sharif PM1, 2 ; Rezaei N3, 4, 5
Authors
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Authors Affiliations
  1. 1. Cancer Immunology Project (CIP), Universal Scientific Education and Research Network (USERN), Tehran, Iran
  2. 2. School of Medicine, Tehran University of Medical Sciences, Tehran, Iran
  3. 3. Research Center for Immunodeficiencies, Children's Medical Cen-ter, Tehran University of Medical Sciences, Tehran, Iran
  4. 4. Department of Immunology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran
  5. 5. Cancer Immunology Project (CIP), Universal Scientific Education and Research Network (USERN), Sheffield, United Kingdom

Source: Current Pharmaceutical Design Published:2021


Abstract

Glioblastoma multiforme (GBM) is the most common malignant brain tumor in adults, causing many deaths each year. The life expectancy of patients from the time of diagnosis does not exceed 15 months. Tumoral cells are generally surrounded by a bed of tumor microenvironment (TME), composed of various components such as different immune cells, stromal cells, and blood vessels. Previous studies on the treatment of this tumor have generally focused on cancerous cells and, therefore, have introduced conventional therapies for eradicating this tumor, including maximal safe surgery, chemotherapy with temozolomide (TMZ), and radio-therapy. Despite treatment with this method, tumors almost always recur, and life expectancy has not increased much. Recently, due to the discovery of the various roles of immune cells (including tumor-associated macrophages or TAMs) in the pathogenesis of this disease, the path of studies has moved towards targeting them as a treatment for glioblastoma. In this review, we aimed to investigate recent studies on the different roles of TME components, the role of TAM in the pathogenesis, and novel methods that target TAMs, including induction of TAM repolarization, inhibition of TAM-produced cytokines, and prohibition of immune system suppression induced by TAMs. In this regard, various targets, including colony-stimulating factor-1 (CS-F-1) receptors, Nuclear factor-kappa B (NF-κB), or chemokine receptor (CXCR) pathways, are investigated. © 2021 Bentham Science Publishers.
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