Frequent somatic mutations and homozygous deletions of the p16 (MTS1) gene in pancreatic adenocarcinoma
β Scribed by Caldas, Carlos; Hahn, Stephan A.; da Costa, Luis T.; Redston, Mark S.; Schutte, Mieke; Seymour, Albert B.; Weinstein, Craig L.; Hruban, Ralph H.; Yeo, Charles J.; Kern, Scott E.
- Book ID
- 109917894
- Publisher
- Nature Publishing Group
- Year
- 1994
- Tongue
- English
- Weight
- 668 KB
- Volume
- 8
- Category
- Article
- ISSN
- 1061-4036
No coin nor oath required. For personal study only.
π SIMILAR VOLUMES
Deletion of all or part of chromosome 9 is a well-described genetic alteration in bladder tumors. It has been proposed that inactivation of a tumor-suppressor gene on chromosome 9 is an important event in tumor development. Recent reports have supported cyclin-dependent kinase inhibitor 2 (CDKN2, al
The tumor suppressor gene CDKN2 (p16/MTS1) resides on chromosome 9p21 and encodes a 16 kDa inhibitor of the cyclin-dependent kinases. Inactivation of CDKN2 by homozygous deletion, point mutation, and recently described aberrant methylation in the 5' promoter region may increase progression through t
Loss of heterozygosity on chromosome 9 has been reported in a variety of human cancers. The cyclin-dependent kinase inhibitor p16 gene, mapped on chromosome 9p21, is presumed to be the tumor-suppressor gene localized in this chromosome. The aim of our study was to determine, in 26 Barrett's adenocar