Abstract:
:The cell-cycle regulator p16 inhibits the complex cdk4-cyclin D1 and controls G1-S transition. In human tumors, p16 inactivation is often accomplished by homozygous deletion (HD) of its encoding gene, CDKN2A. Methylation of the 5' CpG island promoter has been proposed as an alternative mechanism of inactivation. Expression of p16, CDKN2A HD and 5' CDKN2A CpG island methylation was studied in 25 oligodendrogliomas by immunohistochemistry and PCR amplification. Ten oligodendrogliomas were p16-immunonegative, and CDKN2A HD was determined in 8 of these cases. In the 2 immunonegative cases without HD, no CpG island methylation was found. The absence of CpG island methylation in the p16-immunonegative cases without HD suggests either non-genetic regulation of p16 or different genetic changes. CDKN2A HD did not correlate with histological grading (p = n.s.); however, it showed a correlation with survival (p = 0.03), supporting an important role of CDKN2A in the prognosis of oligodendrogliomas.
journal_name
Int J Cancerjournal_title
International journal of cancerauthors
Bortolotto S,Chiadò-Piat L,Cavalla P,Bosone I,Chiò A,Mauro A,Schiffer Ddoi
10.1002/1097-0215(20001115)88:4<554::aid-ijc6>3.0.keywords:
subject
Has Abstractpub_date
2000-11-15 00:00:00pages
554-7issue
4eissn
0020-7136issn
1097-0215pii
10.1002/1097-0215(20001115)88:4<554::AID-IJC6>3.0.journal_volume
88pub_type
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