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....

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Hauptverfasser: Giordano, Frank Anton (VerfasserIn) , Link, Barbara (VerfasserIn) , Umansky, Viktor (VerfasserIn) , Herskind, Carsten (VerfasserIn)
Dokumenttyp: Article (Journal)
Sprache:Englisch
Veröffentlicht: 26 February 2019
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
Volltext
Verfasserangaben:Frank A. Giordano, Barbara Link, Martin Glas, Ulrich Herrlinger, Frederik Wenz, Viktor Umansky, J. Martin Brown and Carsten Herskind
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Zusammenfassung: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.
Beschreibung:Gesehen am 14.11.2019
Beschreibung:Online Resource
ISSN:2072-6694
DOI:10.3390/cancers11030272