Targeting the post-irradiation tumor microenvironment in glioblastoma via inhibition of CXCL12
Radiotherapy is a mainstay in glioblastoma therapy as it not only directly targets tumor cells but also depletes the tumor microvasculature. The resulting intra-tumoral hypoxia initiates a chain of events that ultimately leads to re-vascularization, immunosuppression and, ultimately, tumor-regrowth....
Gespeichert in:
| Hauptverfasser: | , , , |
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| Dokumenttyp: | Article (Journal) |
| Sprache: | Englisch |
| Veröffentlicht: |
26 February 2019
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| In: |
Cancers
Year: 2019, Jahrgang: 11, Heft: 3 |
| ISSN: | 2072-6694 |
| DOI: | 10.3390/cancers11030272 |
| Online-Zugang: | Verlag, Volltext: https://doi.org/10.3390/cancers11030272 Verlag: https://www.mdpi.com/2072-6694/11/3/272 
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| Verfasserangaben: | Frank A. Giordano, Barbara Link, Martin Glas, Ulrich Herrlinger, Frederik Wenz, Viktor Umansky, J. Martin Brown and Carsten Herskind |
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| 520 | |a Radiotherapy is a mainstay in glioblastoma therapy as it not only directly targets tumor cells but also depletes the tumor microvasculature. The resulting intra-tumoral hypoxia initiates a chain of events that ultimately leads to re-vascularization, immunosuppression and, ultimately, tumor-regrowth. The key component of this cascade is overexpression of the CXC-motive chemokine ligand 12 (CXCL12), formerly known as stromal-cell derived factor 1 (SDF-1). We here review the role of CXCL12 in recruitment of pro-vasculogenic and immunosuppressive cells and give an overview on future and current drugs that target this axis. | ||
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