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Tumor-promoting myeloid cells in the pathogenesis of human oncoviruses: potential targets for immunotherapy

Oncoviruses, known as cancer-causing viruses, are typically involved in cancer progression by inhibiting tumor suppressor pathways and uncontrolled cell division. Myeloid cells are the most frequent populations recruited to the tumor microenvironment (TME) and play a critical role in cancer developm...

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Autores principales: Aghamajidi, Azin, Farhangnia, Pooya, Pashangzadeh, Salar, Damavandi, Amirmasoud Rayati, Jafari, Reza
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9608890/
https://www.ncbi.nlm.nih.gov/pubmed/36303138
http://dx.doi.org/10.1186/s12935-022-02727-3
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author Aghamajidi, Azin
Farhangnia, Pooya
Pashangzadeh, Salar
Damavandi, Amirmasoud Rayati
Jafari, Reza
author_facet Aghamajidi, Azin
Farhangnia, Pooya
Pashangzadeh, Salar
Damavandi, Amirmasoud Rayati
Jafari, Reza
author_sort Aghamajidi, Azin
collection PubMed
description Oncoviruses, known as cancer-causing viruses, are typically involved in cancer progression by inhibiting tumor suppressor pathways and uncontrolled cell division. Myeloid cells are the most frequent populations recruited to the tumor microenvironment (TME) and play a critical role in cancer development and metastasis of malignant tumors. Tumor-infiltrating myeloid cells, including tumor-associated macrophages (TAMs), myeloid-derived suppressor cells (MDSCs), tumor-associated dendritic cells (TADCs), and tumor-associated neutrophils (TANs) exert different states from anti-tumorigenic to pro-tumorigenic phenotypes in TME. Although their role in the anti-tumorigenic state is well introduced, their opposing roles, pro-tumorigenic activities, such as anti-inflammatory cytokine and reactive oxygen species (ROS) production, should not be ignored since they result in inflammation, tumor progression, angiogenesis, and evasion. Since the blockade of these cells had promising results against cancer progression, their inhibition might be helpful in various cancer immunotherapies. This review highlights the promoting role of tumor-associated myeloid cells (TAMCs) in the pathophysiology of human virus tumorigenesis.
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spelling pubmed-96088902022-10-28 Tumor-promoting myeloid cells in the pathogenesis of human oncoviruses: potential targets for immunotherapy Aghamajidi, Azin Farhangnia, Pooya Pashangzadeh, Salar Damavandi, Amirmasoud Rayati Jafari, Reza Cancer Cell Int Review Oncoviruses, known as cancer-causing viruses, are typically involved in cancer progression by inhibiting tumor suppressor pathways and uncontrolled cell division. Myeloid cells are the most frequent populations recruited to the tumor microenvironment (TME) and play a critical role in cancer development and metastasis of malignant tumors. Tumor-infiltrating myeloid cells, including tumor-associated macrophages (TAMs), myeloid-derived suppressor cells (MDSCs), tumor-associated dendritic cells (TADCs), and tumor-associated neutrophils (TANs) exert different states from anti-tumorigenic to pro-tumorigenic phenotypes in TME. Although their role in the anti-tumorigenic state is well introduced, their opposing roles, pro-tumorigenic activities, such as anti-inflammatory cytokine and reactive oxygen species (ROS) production, should not be ignored since they result in inflammation, tumor progression, angiogenesis, and evasion. Since the blockade of these cells had promising results against cancer progression, their inhibition might be helpful in various cancer immunotherapies. This review highlights the promoting role of tumor-associated myeloid cells (TAMCs) in the pathophysiology of human virus tumorigenesis. BioMed Central 2022-10-27 /pmc/articles/PMC9608890/ /pubmed/36303138 http://dx.doi.org/10.1186/s12935-022-02727-3 Text en © The Author(s) 2022 https://creativecommons.org/licenses/by/4.0/Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) . The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/ (https://creativecommons.org/publicdomain/zero/1.0/) ) applies to the data made available in this article, unless otherwise stated in a credit line to the data.
spellingShingle Review
Aghamajidi, Azin
Farhangnia, Pooya
Pashangzadeh, Salar
Damavandi, Amirmasoud Rayati
Jafari, Reza
Tumor-promoting myeloid cells in the pathogenesis of human oncoviruses: potential targets for immunotherapy
title Tumor-promoting myeloid cells in the pathogenesis of human oncoviruses: potential targets for immunotherapy
title_full Tumor-promoting myeloid cells in the pathogenesis of human oncoviruses: potential targets for immunotherapy
title_fullStr Tumor-promoting myeloid cells in the pathogenesis of human oncoviruses: potential targets for immunotherapy
title_full_unstemmed Tumor-promoting myeloid cells in the pathogenesis of human oncoviruses: potential targets for immunotherapy
title_short Tumor-promoting myeloid cells in the pathogenesis of human oncoviruses: potential targets for immunotherapy
title_sort tumor-promoting myeloid cells in the pathogenesis of human oncoviruses: potential targets for immunotherapy
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9608890/
https://www.ncbi.nlm.nih.gov/pubmed/36303138
http://dx.doi.org/10.1186/s12935-022-02727-3
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