Tumor-Associated Macrophages in Glioma: Friend or Foe?. (8th May 2013)
- Record Type:
- Journal Article
- Title:
- Tumor-Associated Macrophages in Glioma: Friend or Foe?. (8th May 2013)
- Main Title:
- Tumor-Associated Macrophages in Glioma: Friend or Foe?
- Authors:
- Kennedy, Benjamin C.
Showers, Christopher R.
Anderson, David E.
Anderson, Lisa
Canoll, Peter
Bruce, Jeffrey N.
Anderson, Richard C. E. - Other Names:
- Hara Akira Academic Editor.
- Abstract:
- Abstract : Tumor-associated macrophages (TAMs) contribute substantially to the tumor mass of gliomas and have been shown to play a major role in the creation of a tumor microenvironment that promotes tumor progression. Shortcomings of attempts at antiglioma immunotherapy may result from a failure to adequately address these effects. Emerging evidence supports an independent categorization of glioma TAMs as alternatively activated M2-type macrophages, in contrast to classically activated proinflammatory M1-type macrophages. These M2-type macrophages exert glioma-supportive effects through reduced anti-tumor functions, increased expression of immunosuppressive mediators, and nonimmune tumor promotion through expression of trophic and invasion-facilitating substances. Much of our work has demonstrated these features of glioma TAMs, and together with the supporting literature will be reviewed here. Additionally, the dynamics of glioma cell-TAM interaction over the course of tumor development remain poorly understood; our efforts to elucidate glioma cell-TAM dynamics are summarized. Finally, the molecular pathways which underlie M2-type TAM polarization and gene expression similarly require further investigation, and may present the most potent targets for immunotherapeutic intervention. Highlighting recent evidence implicating the transcription factor STAT3 in immunosuppressive tumorigenic glioma TAMs, we advocate for gene array-based approaches to identify yet unappreciatedAbstract : Tumor-associated macrophages (TAMs) contribute substantially to the tumor mass of gliomas and have been shown to play a major role in the creation of a tumor microenvironment that promotes tumor progression. Shortcomings of attempts at antiglioma immunotherapy may result from a failure to adequately address these effects. Emerging evidence supports an independent categorization of glioma TAMs as alternatively activated M2-type macrophages, in contrast to classically activated proinflammatory M1-type macrophages. These M2-type macrophages exert glioma-supportive effects through reduced anti-tumor functions, increased expression of immunosuppressive mediators, and nonimmune tumor promotion through expression of trophic and invasion-facilitating substances. Much of our work has demonstrated these features of glioma TAMs, and together with the supporting literature will be reviewed here. Additionally, the dynamics of glioma cell-TAM interaction over the course of tumor development remain poorly understood; our efforts to elucidate glioma cell-TAM dynamics are summarized. Finally, the molecular pathways which underlie M2-type TAM polarization and gene expression similarly require further investigation, and may present the most potent targets for immunotherapeutic intervention. Highlighting recent evidence implicating the transcription factor STAT3 in immunosuppressive tumorigenic glioma TAMs, we advocate for gene array-based approaches to identify yet unappreciated expression regulators and effector molecules important to M2-type glioma TAMs polarization and function within the glioma tumor microenvironment. … (more)
- Is Part Of:
- Journal of oncology. Volume 2013(2013)
- Journal:
- Journal of oncology
- Issue:
- Volume 2013(2013)
- Issue Display:
- Volume 2013, Issue 2013 (2013)
- Year:
- 2013
- Volume:
- 2013
- Issue:
- 2013
- Issue Sort Value:
- 2013-2013-2013-0000
- Page Start:
- Page End:
- Publication Date:
- 2013-05-08
- Subjects:
- Oncology -- Research -- Periodicals
Tumors -- Periodicals
Neoplasms
Oncology -- Research
Tumors
Periodicals
Periodicals
616.994 - Journal URLs:
- https://www.hindawi.com/journals/jo/ ↗
http://www.pubmedcentral.nih.gov/tocrender.fcgi?journal=859&action=archive ↗ - DOI:
- 10.1155/2013/486912 ↗
- Languages:
- English
- ISSNs:
- 1687-8450
- Deposit Type:
- Legaldeposit
- View Content:
- Available online (eLD content is only available in our Reading Rooms) ↗
- Physical Locations:
- British Library HMNTS - ELD Digital store
- Ingest File:
- 17171.xml