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Related Concept Videos

Cancer-Critical Genes I: Proto-oncogenes01:33

Cancer-Critical Genes I: Proto-oncogenes

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.
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...
Cancer-Critical Genes I: Proto-oncogenes01:33

Cancer-Critical Genes I: Proto-oncogenes

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.
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...
The Retinoblastoma Gene01:20

The Retinoblastoma Gene

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.
The first-ever tumor suppressor gene called Rb was identified in retinoblastoma - a rare eye tumor in children. In inherited forms of the disease, a child inherits one defective copy of the Rb gene, which predisposes them to retinoblastoma. However,...

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Related Experiment Video

Updated: Jun 1, 2026

Isolation and Flow Cytometric Analysis of Glioma-infiltrating Peripheral Blood Mononuclear Cells
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Isolation and Flow Cytometric Analysis of Glioma-infiltrating Peripheral Blood Mononuclear Cells

Published on: November 28, 2015

Protooncogene expression in human glioma derived cell-lines.

W Hamel1, M Westphal, H Shepard

  • 1UNIV HOSP EPPENDORF,DEPT NEUROL SURG,BRAIN TUMOUR BIOL LAB,MARTINISTR 52,W-2000 HAMBURG 20,GERMANY. GENENTECH INC,DEPT DEV BIOL,SAN FRANCISCO,CA 94080.

International Journal of Oncology
|May 18, 2011
PubMed
Summary

This study investigated growth factor and receptor expression in human glioma cell lines. Findings indicate multiple growth factor/receptor systems are simultaneously active in these cancer cells, suggesting potential therapeutic targets.

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Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Signaling

Background:

  • Growth factor/ligand interactions are crucial in cancer development.
  • Understanding these interactions in glioma is vital for targeted therapies.

Purpose of the Study:

  • To investigate the expression of various growth factors and their receptors in human glioma cell lines.
  • To determine the co-activation patterns of these signaling pathways in glioma.

Main Methods:

  • Reverse Transcription Polymerase Chain Reaction (RT-PCR) for SCF expression.
  • Northern blot analysis for c-kit, PDGF receptors, TGF-alpha, and PDGF B/c-sis.
  • Flow cytometry (FACS) for Epidermal Growth Factor Receptor (EGFR) and p185HER2.
  • Differential PCR to assess EGFR gene amplification.

Main Results:

  • SCF expression detected in 20/24 glioma cell lines.
  • Receptors c-kit, PDGF alpha-receptor, PDGF beta-receptor, TGF-alpha, and PDGF B/c-sis were expressed in a significant proportion of cell lines.
  • EGFR and p185HER2 were ubiquitously detected (21/21 and 15/21, respectively).
  • Moderate EGFR overexpression and higher p185HER2 levels were observed in some lines.
  • Loss of EGFR gene amplification occurred during in vitro culturing in 3/18 lines.

Conclusions:

  • Human glioma cell lines exhibit simultaneous activation of multiple growth factor/receptor systems.
  • This co-activation suggests complex signaling networks driving glioma progression.
  • Findings highlight potential for targeting multiple pathways in glioma treatment.