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
Inactivation of p16 by methylation in human lung adenocarcinoma
โ Scribed by Divine, Kevin K.; Gilland, Frank D.; Stidley, Christine A.; Bocklage, Therese J.; Schwartz, Ann; Cook, Dennis L.; Belinsky, Steven A.
- Book ID
- 109830388
- Publisher
- Nature Publishing Group
- Year
- 2001
- Tongue
- English
- Weight
- 40 KB
- Volume
- 27
- Category
- Article
- ISSN
- 1061-4036
- DOI
- 10.1038/87058
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The p16 (CDKN2/MTS-1/INK4A) tumor-suppressor gene is frequently inactivated by DNA methylation in lung carcinomas. To clarify whether background anthracosis may play a role in DNA methylation and inactivation of the p16 gene, we examined DNA methylation of the p16-promoter region by methylation-spec