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Frequent inactivation of the p16 gene in human pituitary tumors by gene methylation

✍ Scribed by Michael Woloschak; Aiqin Yu; Kalmon D. Post

Publisher: John Wiley and Sons
Year: 1997
Tongue: English
Weight: 87 KB
Volume: 19
Category: Article
ISSN: 0899-1987
DOI: 10.1002/(sici)1098-2744(199708)19:4<221::aid-mc1>3.0.co;2-f

No coin nor oath required. For personal study only.

✦ Synopsis

Rodent models of pituitary tumorigenesis have implicated the retinoblastoma (Rb) pathway in the development of pituitary tumors. Previously, we reported that loss of p16 expression rather than loss of Rb occurs in most human pituitary adenomas. This alteration in these tumors is not associated with p16 mutation or frequent homozygous p16 gene loss. Our laboratory has now demonstrated that in most human pituitary tumors, the 5´ CpG island of the p16 gene is extensively methylated. The high frequency of p16 gene methylation in human pituitary tumors suggests that this alteration is an early and perhaps required event in pituitary cell transformation.

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