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MINI REVIEW article

Front. Oncol.

Sec. Neuro-Oncology and Neurosurgical Oncology

Impact of Corticosteroid Administration on Glioblastoma Progression Before and After Adjuvant Treatments: Recent Updates on Contradictory Findings and Mechanistic Interactions

Provisionally accepted
Maher  KurdiMaher Kurdi1*Ali  KabliAli Kabli1Alaa  AlkhotaniAlaa Alkhotani2Amal  AlkhotaniAmal Alkhotani2Rakan  BokhariRakan Bokhari1Zayd  JastaniahZayd Jastaniah1Razan  AmjadRazan Amjad1Huda  AltoukhiHuda Altoukhi1Taghreed  AlsinaniTaghreed Alsinani3Hussain  AlamoudiHussain Alamoudi4Saleh  BaeesaSaleh Baeesa5
  • 1King Abdulaziz University, Jeddah, Saudi Arabia
  • 2Umm Al-Qura University, Mecca, Saudi Arabia
  • 3King Fahad Hospital Jeddah, Jeddah, Saudi Arabia
  • 4East Jeddah General Hospital, Jeddah, Saudi Arabia
  • 5King Faisal Specialist Hospital & Research Centre - Jeddah, Jeddah, Saudi Arabia

The final, formatted version of the article will be published soon.

Corticosteroids, particularly dexamethasone (DEX), are widely used in the supportive management of glioblastoma and grade 4 astrocytoma because of their rapid ef]icacy in reducing vasogenic cerebral edema and alleviating neurological symptoms. Despite these bene]its, their impact on tumor biology and treatment response remains highly controversial. While experimental studies have reported anti-proliferative and anti-migratory effects of DEX in glioma models, accumulating clinical and translational evidence suggests detrimental interactions with radiotherapy (RT) and temozolomide (TMZ), particularly when steroids are administered at higher doses or during RT. Proposed mechanisms include induction of chemoresistance, suppression of antitumor immune responses, and modulation of DNA damage repair pathways within the tumor microenvironment. Recent data implicate steroid receptor coactivator-1 (SRC-1) as a key molecular mediator linking corticosteroid signaling to immune regulation and tumor recurrence, highlighting a novel microenvironmental mechanism independent of steroid dose. Emerging therapeutic strategies, including agents targeting epigenetic regulators, metabolic pathways, or repurposed drugs such as Riluzole, Metformin, Mifepristone, and Chlorpromazine, show promise in mitigating steroid-associated resistance to TMZ. Collectively, these ]indings emphasize the complex, context-dependent role of corticosteroids in glioblastoma or grade 4 astrocytoma and emphasize the need for optimized dosing, timing, and integrated treatment strategies to improve patient outcomes.

Keywords: corticosteroids, Dexamethasone, Glioblastoma, Grade 4 astrocytoma, progression, temozolomide resistance

Received: 24 Dec 2025; Accepted: 10 Feb 2026.

Copyright: © 2026 Kurdi, Kabli, Alkhotani, Alkhotani, Bokhari, Jastaniah, Amjad, Altoukhi, Alsinani, Alamoudi and Baeesa. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

* Correspondence: Maher Kurdi

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