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Related Experiment Video

Updated: Mar 24, 2026

Transposon Mediated Integration of Plasmid DNA into the Subventricular Zone of Neonatal Mice to Generate Novel Models of Glioblastoma

Transposon Mediated Integration of Plasmid DNA into the Subventricular Zone of Neonatal Mice to Generate Novel Models of Glioblastoma

Published on: February 22, 2015

Glioblastoma.

Hans-Georg Wirsching¹, Evanthia Galanis², Michael Weller¹

¹Department of Neurology, University Hospital Zurich, Zurich, Switzerland.

Handbook of Clinical Neurology

|March 8, 2016

Summary

This summary is machine-generated.

Glioblastoma, an aggressive brain tumor, is classified by specific features and molecular changes. Treatment involves surgery, radiation, and chemotherapy, with O(6)-methylguanyl DNA methyltransferase (MGMT) promoter methylation guiding therapy.

Keywords:

angiogenesis glioblastoma glioma-initiating cell immunotherapy molecular subtype radiotherapy temozolomide

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Last Updated: Mar 24, 2026

Transposon Mediated Integration of Plasmid DNA into the Subventricular Zone of Neonatal Mice to Generate Novel Models of Glioblastoma

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Published on: February 22, 2015

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Published on: November 28, 2015

Translational Orthotopic Models of Glioblastoma Multiforme

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Published on: February 17, 2023

Area of Science:

Neuro-oncology
Molecular pathology
Cancer biology

Background:

Glioblastoma is the most aggressive primary adult brain tumor, WHO grade IV.
Characterized by necrosis and endothelial proliferation.
Secondary glioblastoma evolves from lower-grade gliomas.

Purpose of the Study:

To define the histopathologic and molecular features of glioblastoma.
To outline current treatment strategies and emerging therapeutic targets.
To discuss the role of molecular markers in glioblastoma classification and treatment.

Main Methods:

Histopathologic analysis for necrosis and endothelial proliferation.
Molecular profiling for IDH mutations, RTK/RAS/PI3K, p53, and RB signaling.
Assessment of O(6)-methylguanyl DNA methyltransferase (MGMT) promoter methylation.

Main Results:

IDH mutations define a subset of glioblastomas with younger age and better prognosis.
Glioblastomas typically exhibit mutations in RTK/RAS/PI3K, p53, and RB pathways.
MGMT promoter methylation predicts response to alkylating chemotherapy (temozolomide).

Conclusions:

Glioblastoma classification relies on histopathology and molecular markers like IDH and MGMT.
Standard treatments include surgery, radiotherapy, and chemotherapy.
Future directions involve targeting molecular pathways and immunotherapy.