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Expression of cyclin D2, P53, Rb and ATM cell cycle genes in brain tumors

Majid Kheirollahi1, Masoud Mehr-Azin, Naser Kamalian

  • 1Department of Medical Genetics, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran. mkheirollahi@tums.ac.ir

Medical Oncology (Northwood, London, England)
|January 16, 2010
PubMed

Insights

Cell cycle genes cyclin D2, P53, Rb, and ATM show varied mRNA expression in brain tumors. Their expression differs between astrocytoma and meningioma, with complex regulation across tumor grades.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Cell cycle genes, including cyclin D2, P53, Rb, and ATM, are crucial regulators of cell growth and proliferation.
  • Understanding their expression patterns in brain tumors is essential for comprehending tumor development and progression.

Purpose of the Study:

  • To investigate the differential mRNA expression of cyclin D2, P53, Rb, and ATM in astrocytoma and meningioma brain tumors.
  • To analyze the correlation of these gene expressions with different tumor grades.

Main Methods:

  • Extraction of mRNA from 52 brain tumor samples (astrocytoma and meningioma).
  • Quantification of cyclin D2, P53, Rb, and ATM mRNA expression using real-time quantitative reverse-transcription polymerase chain reaction (RT-qPCR).
  • Comparative analysis of gene expression between tumor types and grades.

Main Results:

  • Astrocytoma tumors exhibited higher mRNA expression of cyclin D2, P53, Rb, and ATM compared to meningioma tumors.
  • Higher grades (III and IV) of astrocytoma showed upregulation of cyclin D2 and ATM, but downregulation of P53 and Rb.
  • Meningioma grade II showed significant downregulation of all studied genes compared to grade I.
  • A strong positive correlation was observed for these genes in lower grades of both tumor types.

Conclusions:

  • The mRNA expression levels of cyclin D2, P53, Rb, and ATM vary significantly between astrocytoma and meningioma.
  • Tumor grade influences the expression patterns of these cell cycle genes, indicating complex regulatory mechanisms.
  • These findings suggest that the interaction models of these genes are not uniform across different brain tumor types and grades.

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