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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Bibliographic Details
Main Authors: Giordano, Frank Anton (Author) , Link, Barbara (Author) , Umansky, Viktor (Author) , Herskind, Carsten (Author)
Format: Article (Journal)
Language:English
Published: 26 February 2019
In: Cancers
Year: 2019, Volume: 11, Issue: 3
ISSN:2072-6694
DOI:10.3390/cancers11030272
Online Access:Verlag, Volltext: https://doi.org/10.3390/cancers11030272
Verlag: https://www.mdpi.com/2072-6694/11/3/272
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Author Notes:Frank A. Giordano, Barbara Link, Martin Glas, Ulrich Herrlinger, Frederik Wenz, Viktor Umansky, J. Martin Brown and Carsten Herskind
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Summary: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.
Item Description:Gesehen am 14.11.2019
Physical Description:Online Resource
ISSN:2072-6694
DOI:10.3390/cancers11030272