Moreover, inflammation is crucial for GBM progression.
Therefore, Wnt/β-catenin pathway is postulated as a promising target in GBM therapy. Without the protective role of its natural antagonists, Wnt pathway is hyperactivated, contributing to the maintenance of GBM cells stemness, invasiveness, and angiogenesis, as well as chemio- and radioresistance. As we and others have previously shown, hyperactivation of this signaling pathway is mainly caused by promoter methylation of its inhibitors. One of the most critical oncogenic drivers of GBM is the Wnt/β-catenin pathway. Novel therapies, drug targets, and drug combinations are needed to prolong GBM patients lifespan. Despite surgical resection followed by radio- and chemotherapy, GBM tends to recur and only fewer than 5% of patients survive 5 years after diagnosis. It is highly heterogeneous and driven by diverse genetic, epigenetic, and developmental programs.
GBM represents the most aggressive and the most common primary brain tumor in adults. The Creative Commons Public Domain Dedication waiver ( ) applies to the data made available in this article, unless otherwise stated in a credit line to the data. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made.
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