Shu Hang, Zhou Dong, Li Zhaojie, Lin Zhijun
Department of Neurosurgery, Guangdong Provincial People's Hospital, Guangzhou 510080, China.
Zhonghua Yu Fang Yi Xue Za Zhi. 2002 Dec;36(7):517-8.
To study the relationship among p16, genesis, and development of brain gliomas.
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.
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.
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.
