Role of inflammatory mediators, macrophages, and neutrophils in glioma maintenance and progression: mechanistic understanding and potential therapeutic applications
Gliomas are the most common, highly malignant, and deadliest forms of brain tumors. These intra-cranial solid tumors are comprised of both cancerous and non-cancerous cells, which contribute to tumor development, progression, and resistance to the therapeutic regimen. A variety of soluble inflammato...
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| Format: | Article |
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MDPI AG
2021
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| Online Access: | http://psasir.upm.edu.my/id/eprint/94990/ |
| _version_ | 1848862046804770816 |
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| author | Basheer, Abdul Samad Abas, Faridah Othman, Iekhsan Naidu, Rakesh |
| author_facet | Basheer, Abdul Samad Abas, Faridah Othman, Iekhsan Naidu, Rakesh |
| author_sort | Basheer, Abdul Samad |
| building | UPM Institutional Repository |
| collection | Online Access |
| description | Gliomas are the most common, highly malignant, and deadliest forms of brain tumors. These intra-cranial solid tumors are comprised of both cancerous and non-cancerous cells, which contribute to tumor development, progression, and resistance to the therapeutic regimen. A variety of soluble inflammatory mediators (e.g., cytokines, chemokines, and chemotactic factors) are secreted by these cells, which help in creating an inflammatory microenvironment and contribute to the various stages of cancer development, maintenance, and progression. The major tumor infiltrating immune cells of the tumor microenvironment include TAMs and TANs, which are either recruited peripherally or present as brain-resident macrophages (microglia) and support stroma for cancer cell expansion and invasion. These cells are highly plastic in nature and can be polarized into different phenotypes depending upon different types of stimuli. During neuroinflammation, glioma cells interact with TAMs and TANs, facilitating tumor cell proliferation, survival, and migration. Targeting inflammatory mediators along with the reprogramming of TAMs and TANs could be of great importance in glioma treatment and may delay disease progression. In addition, an inhibition of the key signaling pathways such as NF-κB, JAK/STAT, MAPK, PI3K/Akt/mTOR, and TLRs, which are activated during neuroinflammation and have an oncogenic role in glioblastoma (GBM), can exert more pronounced anti-glioma effects. |
| first_indexed | 2025-11-15T13:10:48Z |
| format | Article |
| id | upm-94990 |
| institution | Universiti Putra Malaysia |
| institution_category | Local University |
| last_indexed | 2025-11-15T13:10:48Z |
| publishDate | 2021 |
| publisher | MDPI AG |
| recordtype | eprints |
| repository_type | Digital Repository |
| spelling | upm-949902023-02-16T06:59:02Z http://psasir.upm.edu.my/id/eprint/94990/ Role of inflammatory mediators, macrophages, and neutrophils in glioma maintenance and progression: mechanistic understanding and potential therapeutic applications Basheer, Abdul Samad Abas, Faridah Othman, Iekhsan Naidu, Rakesh Gliomas are the most common, highly malignant, and deadliest forms of brain tumors. These intra-cranial solid tumors are comprised of both cancerous and non-cancerous cells, which contribute to tumor development, progression, and resistance to the therapeutic regimen. A variety of soluble inflammatory mediators (e.g., cytokines, chemokines, and chemotactic factors) are secreted by these cells, which help in creating an inflammatory microenvironment and contribute to the various stages of cancer development, maintenance, and progression. The major tumor infiltrating immune cells of the tumor microenvironment include TAMs and TANs, which are either recruited peripherally or present as brain-resident macrophages (microglia) and support stroma for cancer cell expansion and invasion. These cells are highly plastic in nature and can be polarized into different phenotypes depending upon different types of stimuli. During neuroinflammation, glioma cells interact with TAMs and TANs, facilitating tumor cell proliferation, survival, and migration. Targeting inflammatory mediators along with the reprogramming of TAMs and TANs could be of great importance in glioma treatment and may delay disease progression. In addition, an inhibition of the key signaling pathways such as NF-κB, JAK/STAT, MAPK, PI3K/Akt/mTOR, and TLRs, which are activated during neuroinflammation and have an oncogenic role in glioblastoma (GBM), can exert more pronounced anti-glioma effects. MDPI AG 2021-08-23 Article PeerReviewed Basheer, Abdul Samad and Abas, Faridah and Othman, Iekhsan and Naidu, Rakesh (2021) Role of inflammatory mediators, macrophages, and neutrophils in glioma maintenance and progression: mechanistic understanding and potential therapeutic applications. Cancers, 13 (16). pp. 1-31. ISSN 2072-6694 https://www.mdpi.com/2072-6694/13/16/4226 10.3390/cancers13164226 |
| spellingShingle | Basheer, Abdul Samad Abas, Faridah Othman, Iekhsan Naidu, Rakesh Role of inflammatory mediators, macrophages, and neutrophils in glioma maintenance and progression: mechanistic understanding and potential therapeutic applications |
| title | Role of inflammatory mediators, macrophages, and neutrophils in glioma maintenance and progression: mechanistic understanding and potential therapeutic applications |
| title_full | Role of inflammatory mediators, macrophages, and neutrophils in glioma maintenance and progression: mechanistic understanding and potential therapeutic applications |
| title_fullStr | Role of inflammatory mediators, macrophages, and neutrophils in glioma maintenance and progression: mechanistic understanding and potential therapeutic applications |
| title_full_unstemmed | Role of inflammatory mediators, macrophages, and neutrophils in glioma maintenance and progression: mechanistic understanding and potential therapeutic applications |
| title_short | Role of inflammatory mediators, macrophages, and neutrophils in glioma maintenance and progression: mechanistic understanding and potential therapeutic applications |
| title_sort | role of inflammatory mediators, macrophages, and neutrophils in glioma maintenance and progression: mechanistic understanding and potential therapeutic applications |
| url | http://psasir.upm.edu.my/id/eprint/94990/ http://psasir.upm.edu.my/id/eprint/94990/ http://psasir.upm.edu.my/id/eprint/94990/ |