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Multiple suppressor gene p16 of human brain gliomas
Hang Shu1, Dong Zhou, Zhaojie Li
1Department of Neurosurgery, Guangdong Provincial People's Hospital, Guangzhou 510080, China.
Objective:
To study the relationship among p16, genesis, and development of brain gliomas.
Methods:
We detected the deletion and point mutation of p16 exon 2 by PCR-TGGE. Methylation sensitivity ristriction enzyme polymerase chain reaction was used to detect whether methylation is correlated with happening of glioma.
Results:
p16 homozygous deletion was detected in 14 of 48 gliomas. No deletions were found in low grade gliomas. Of the 48 gliomas, 5 anaplastic gliomas (WHO grade III) and 9 glioblastomas (WHO grade IV) showed homozygous deletion of exon 2 with a deletion rate of 33.33% (5/15) and 50.00% (9/18) respectively. The mutations of 34 gliomas with p16 positive amplification were detected point mutations in two gliomas, in which one was anaplatic glioma and the other was glioblastoma. Six of the 48 gliomas (12.5%) showed exon1 methylations.
Conclusions:
p16 may play an important role in genesis of brain glioma. The main alteration of p16 in brain gliomas was homozygous deletion of exon 2, the methylation of p16 exon 1 was subcardinal, however, point mutation was rare. The deletion of p16 was found especially in high grade gliomas, so we could propose that it may be the late event of tumor occurrence.
Insights
p16 gene alterations, particularly homozygous deletion in exon 2, are linked to brain glioma development. These changes are more common in high-grade gliomas, suggesting a role in later tumor progression.
Area of Science:
- Neuro-oncology
- Molecular Biology
- Genetics
Background:
- Brain gliomas are primary brain tumors with varied origins.
- The p16 gene is a tumor suppressor gene implicated in various cancers.
- Understanding genetic alterations in p16 is crucial for elucidating glioma pathogenesis.
Purpose of the Study:
- To investigate the relationship between the p16 gene and the genesis and development of brain gliomas.
- To identify specific alterations in the p16 gene associated with different glioma grades.
Main Methods:
- Polymerase chain reaction with temperature gradient gel electrophoresis (PCR-TGGE) was used to detect p16 exon 2 deletions and point mutations.
- Methylation-sensitive restriction enzyme polymerase chain reaction was employed to assess p16 promoter methylation.
Main Results:
- p16 homozygous deletion was observed in 14 out of 48 gliomas, predominantly in anaplastic gliomas (33.33%) and glioblastomas (50.00%).
- No deletions were found in low-grade gliomas.
- Point mutations in p16 were rare (2/34), and methylation of p16 exon 1 occurred in 12.5% of cases.
Conclusions:
- The p16 gene plays a significant role in brain glioma development.
- Homozygous deletion of p16 exon 2 is the primary genetic alteration in gliomas, particularly in high-grade tumors, suggesting it's a late event in tumorigenesis.
- p16 exon 1 methylation and point mutations are less common alterations in glioma.
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