PMID- 9290697 OWN - NLM STAT- MEDLINE DCOM- 19970930 LR - 20191024 IS - 0899-1987 (Print) IS - 0899-1987 (Linking) VI - 19 IP - 4 DP - 1997 Aug TI - Frequent inactivation of the p16 gene in human pituitary tumors by gene methylation. PG - 221-4 AB - 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. FAU - Woloschak, M AU - Woloschak M AD - Department of Medicine, Mount Sinai School of Medicine, New York, New York 10029, USA. FAU - Yu, A AU - Yu A FAU - Post, K D AU - Post KD LA - eng PT - Journal Article PL - United States TA - Mol Carcinog JT - Molecular carcinogenesis JID - 8811105 RN - 0 (Carrier Proteins) RN - 0 (Cyclin-Dependent Kinase Inhibitor p16) RN - 0 (DNA, Neoplasm) SB - IM MH - Adenoma/*genetics/*metabolism MH - Carrier Proteins/biosynthesis/*genetics MH - Cyclin-Dependent Kinase Inhibitor p16 MH - *DNA Methylation MH - DNA, Neoplasm/genetics/*metabolism MH - Exons MH - *Gene Expression Regulation, Neoplastic MH - Humans MH - Pituitary Neoplasms/*genetics/*metabolism MH - Polymerase Chain Reaction EDAT- 1997/08/01 00:00 MHDA- 1997/09/18 00:01 CRDT- 1997/08/01 00:00 PHST- 1997/08/01 00:00 [pubmed] PHST- 1997/09/18 00:01 [medline] PHST- 1997/08/01 00:00 [entrez] AID - 10.1002/(SICI)1098-2744(199708)19:4<221::AID-MC1>3.0.CO;2-F [pii] AID - 10.1002/(sici)1098-2744(199708)19:4<221::aid-mc1>3.0.co;2-f [doi] PST - ppublish SO - Mol Carcinog. 1997 Aug;19(4):221-4. doi: 10.1002/(sici)1098-2744(199708)19:4<221::aid-mc1>3.0.co;2-f.