New Avenues in Radiotherapy of Glioblastoma: from Bench to Bedside
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Neuro-oncology (R Soffietti, Section Editor)
New Avenues in Radiotherapy of Glioblastoma: from Bench to Bedside ValO˜rie GouazO˜-Andersson, PhD1,2,* Elizabeth Cohen-Jonathan Moyal, MD, PhD1,2 Address 1 Radiation Oncology Department, Institut Claudius Regaud-Institut Universitaire du Cancer de Toulouse-Oncopole, Toulouse, France *,2 INSERM UMR1037, Cancer Research of Toulouse, Oncopole, Toulouse, France Email: [email protected]
* Springer Science+Business Media, LLC, part of Springer Nature 2020
This article is part of the Topical Collection on Neuro-oncology Keywords Glioblastoma I Radiotherapy I Resistance I Glioblastoma stem cells
Abstract Purpose of Review This review presents the new updates in treatment by radiotherapy of patients with glioblastoma. Despite the standard treatment, patients with glioblastoma present a relapse quasi-systematic observed in radiation fields with recurrent tumors resistant to therapy. We will highlight new targets involved in radioresistance, discovered in vitro, and that could have an impact in new treatments for glioblastoma, which remains a lethal tumor. Recent Findings So far, clinical studies did not show any efficacy for patients except the one involving tumor-treating fields. For the last decade, it has been discovered within the tumor the presence of a sub-population of glioblastoma stem cells shown to be highly tumorigenic with high plasticity properties and radioresistant and that can explain the high glioblastoma recurrence rate. Summary Recently published studies in glioblastoma stem cells highlighted new pathways that could be targeted concomitantly with radiotherapy in future clinical trials. Moreover, targeted therapies should be adapted to the individual molecular profile of the tumor, during the treatment.
Introduction Glioblastoma multiform (GBM) is the most common and lethal primary brain tumor in adults. Histological
and molecular genetic study of the biopsy is required for GBM diagnosis. Morphologically, GBM is defined as a
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glial brain tumor with features of malignancy that include angiogenesis and local necrosis. The new WHO classification recognizes, in addition to classical GBM, giant cell GBM, gliosarcoma, and epithelioid GBM as histologically defined variants [1]. Based on gene expression signatures, GBM is categorized into three subtypes associated with prognosis values, namely proneural (PN), classical (CL), and mesenchymal (MES) [2]. The MES subtype is the most aggressive and strongly associated with a poor prognosis compared to PN subtype, CL subtype being intermediate. The standard treatment includes safe surgical resection followed by an association of radiotherapy and Temozolomide [3]. MGMT methylation status is the most commonly used biomarker in
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GBM and, studies suggest, may be predictive of the likelihood of patients with GBM to respond to alkylating chemotherapy such as temozolomide. Patients with MGMT-unmethylated GBM are generally known to have a worse prognos
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