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Updated: Aug 25, 2025
Optimization of High Grade Glioma Cell Culture from Surgical Specimens for Use in Clinically Relevant Animal Models and 3D Immunochemistry
Published on: January 7, 2014
[Cell cultures in assessing radioresistance of glioblastomas]
A S Belyashova1, M V Galkin1, N A Antipina1
1Burdenko Neurosurgical Center, Moscow, Russia.
Abstract:
To date, no modern methods of treatment allow overcoming malignant potential of glial neoplasms and significant increase of survival. Analysis of glioblastoma radioresistance using cancer cell cultures is one of the perspective directions, as radiotherapy is standard and available treatment method for these neoplasms. This review summarizes current studies identifying many factors of radioresistance of glial tumors, such as hypoxia, microenvironment and metabolic features of tumor, stem cells, internal heterogeneity of tumor, microRNA, features of cell cycle, DNA damage and reparation. We obtained data on involvement of various molecular pathways in development of radioresistance such as MEK/ERK, c-MYC, PI3K/Akt, PTEN, Wnt, JAK/STAT, Notch, etc. Changes in activity of RAD51 APC, FZD1, LEF1, TCF4, WISP1, p53 and many others are determined in radioresistant cells. Further study of radioresistance pathways will allow development of specific target aptamers and inhibitors.
Insights
Glioblastoma radioresistance is a major challenge, with factors like hypoxia and tumor microenvironment contributing to treatment failure. Understanding these mechanisms is key to developing new therapies that improve patient survival.
Area of Science:
- Oncology
- Radiation Oncology
- Molecular Biology
Background:
- Glioblastoma remains a challenging malignancy with limited treatment options for improving survival.
- Radiotherapy is a standard treatment, but glioblastoma's radioresistance significantly hinders its effectiveness.
Purpose of the Study:
- To review and summarize current research on the factors contributing to glioblastoma radioresistance.
- To identify molecular pathways and cellular mechanisms involved in radioresistance for potential therapeutic targeting.
Main Methods:
- Literature review of studies analyzing glioblastoma radioresistance.
- Analysis of factors including hypoxia, tumor microenvironment, metabolic features, stem cells, and tumor heterogeneity.
- Examination of molecular pathways (e.g., MEK/ERK, PI3K/Akt) and genetic alterations (e.g., p53, RAD51).
Main Results:
- Glioblastoma radioresistance is multifactorial, influenced by intrinsic tumor properties and external microenvironmental cues.
- Key molecular pathways such as MEK/ERK, c-MYC, PI3K/Akt, and Wnt signaling are implicated in radioresistance.
- Specific molecular players like RAD51, p53, and microRNAs show altered activity in radioresistant glioblastoma cells.
Conclusions:
- A comprehensive understanding of glioblastoma radioresistance mechanisms is crucial for developing effective treatments.
- Targeting identified molecular pathways and factors could lead to novel therapeutic strategies, including aptamers and inhibitors.
- Further research into radioresistance pathways promises to enhance glioblastoma treatment outcomes.
