Frequent inactivation of the p16 gene in human pituitary tumors by gene methylation.
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.
Woloschak
M
M
Department of Medicine, Mount Sinai School of Medicine, New York, New York 10029, USA.
Yu
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D000236:Adenoma / Q000235:genetics* / Q000378:metabolism*; D002352:Carrier Proteins / Q000096:biosynthesis / Q000235:genetics*; D019941:Cyclin-Dependent Kinase Inhibitor p16; D019175:DNA Methylation; D004273:DNA, Neoplasm / Q000235:genetics / Q000378:metabolism*; D005091:Exons; D015972:Gene Expression Regulation, Neoplastic; D006801:Humans; D010911:Pituitary Neoplasms / Q000235:genetics* / Q000378:metabolism*; D016133:Polymerase Chain Reaction
D002352:Carrier Proteins; D019941:Cyclin-Dependent Kinase Inhibitor p16; D004273:DNA, Neoplasm