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Updated: Aug 23, 2026

Genome-Wide Analysis of DNA Methylation in Gastrointestinal Cancer
Published on: September 18, 2020
[Methylation and expression analysis of p16(INK4a) and RB genes in meningiomas]
Mi-na Chen1, Qing Mao, Yan-hui Liu
1Department of Infectious Disease, West China Hospital, Sichuan University, Chengdu, Sichuan, 610041 PR China.
Objective:
To investigate the methylation of p16(INK4a) and RB gene, and the expression of p16(INK4a) in meningiomas.
Methods:
Methylation-specific polymerase chain reaction (MSP) was used to detect the methylation of p16(INK4a) and RB in 50 cases of meningiomas, and immunostaining was performed to analyze the protein expression of p16(INK4a) in 25 of those cases.
Results:
No methylation was found in the benign meningiomas, whereas methylation of p16(INK4a)or RB occurred in 6(37.5%) cases of grade II tumors and 4(28.6%) cases of grade III tumors, and among these cases, an atypical meningioma showed methylation of both genes. Thirteen cases showed p16(INK4a) positive expression, but none of them was methylated.
Conclusion:
The methylation of p16(INK4a) or RB is related with the tumorigenesis and progression of atypical and anaplastic meningiomas, and a probable mechanism is that methylation causes the loss of expression and leads to dysfuncation of the p16(INK4a)/cyclin D1/CDK4/RB pathway.
Insights
Methylation of p16(INK4a) or RB genes is linked to meningioma progression. This epigenetic change may cause loss of p16(INK4a) expression, impacting the cell cycle pathway.
Area of Science:
- Oncology
- Epigenetics
- Molecular Biology
Context:
- Meningiomas are primary tumors of the central nervous system.
- Understanding the molecular mechanisms underlying meningioma progression is crucial for diagnosis and treatment.
Purpose:
- To investigate the methylation status of p16(INK4a) and RB genes.
- To analyze p16(INK4a) protein expression in meningiomas.
- To correlate these molecular changes with tumor grade and progression.
Summary:
- Methylation-specific polymerase chain reaction (MSP) and immunostaining were used on 50 meningioma cases.
- No p16(INK4a) or RB methylation was observed in benign meningiomas.
- Methylation of p16(INK4a) or RB was detected in 37.5% of grade II and 28.6% of grade III meningiomas.
- p16(INK4a) expression was observed in 13 cases, none of which showed gene methylation.
Impact:
- Methylation of p16(INK4a) or RB is associated with the tumorigenesis and progression of atypical and anaplastic meningiomas.
- Methylation-induced loss of p16(INK4a) expression likely disrupts the p16(INK4a)/cyclin D1/CDK4/RB pathway.
- These findings provide insights into the epigenetic regulation of meningioma development.
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