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Tumor suppressor genes are normal genes that can slow down cell division, repair DNA mistakes, or program the cells for apoptosis in case of irreparable damage. Hence, they play an essential role in preventing the proliferation of damaged cells.
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Genes usually encode proteins necessary for the proper functioning of a healthy cell. Mutations can often cause changes to the gene expression pattern, thereby altering the phenotype.
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Related Experiment Video

Updated: May 6, 2026

Isolation and Flow Cytometric Analysis of Glioma-infiltrating Peripheral Blood Mononuclear Cells
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Genetic alterations in glioma.

Linda B C Bralten1, Pim J French

  • 1Department of Neurology, Erasmus University Medical Center, Erasmus University Rotterdam, Dr Molewaterplein 50, 3000 CA, Rotterdam, the Netherlands. p.french@erasmusmc.nl.

Cancers
|November 12, 2013
PubMed
Summary

Understanding genetic alterations in gliomas, common brain tumors with poor outcomes, is key. Research highlights affected pathways in glioblastomas and identifies genetic changes in other glioma subtypes for new treatments.

Area of Science:

  • Neuro-oncology
  • Cancer Genetics
  • Molecular Biology

Background:

  • Gliomas are primary brain tumors with poor prognosis.
  • Understanding genetic drivers is crucial for improved patient outcomes and novel therapeutic targets.
  • Recent studies analyzed glioblastoma (GBM) mutations, revealing key affected pathways.

Purpose of the Study:

  • To review common genetic events in glioma initiation and progression.
  • To provide an update on genetic alterations across different glioma subtypes.
  • To suggest future research directions for glioma genetic changes.

Main Methods:

  • Systematic mutation analysis of glioblastomas.
  • Review of genetic alterations in grade II and III gliomas.
  • Identification of affected signaling pathways (receptor tyrosine kinase, TP53, pRB).

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Evaluation of Biomarkers in Glioma by Immunohistochemistry on Paraffin-Embedded 3D Glioma Neurosphere Cultures
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Evaluation of Biomarkers in Glioma by Immunohistochemistry on Paraffin-Embedded 3D Glioma Neurosphere Cultures
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Main Results:

  • Glioblastomas frequently involve the receptor tyrosine kinase, TP53, and pRB pathways.
  • IDH1/2 mutations are common, but other genetic changes in lower-grade gliomas are less understood.
  • TP53 mutations and BRAF gene fusions are noted in specific glioma subtypes.

Conclusions:

  • Genetic alterations significantly contribute to glioma development and progression.
  • Further research into the genetic landscape of all glioma subtypes is needed.
  • Identifying specific genetic changes can lead to targeted therapies and improved glioma patient prognosis.