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Frequent mutations of CDKN2 in primary pancreatic adenocarcinomas

✍ Scribed by Detlef Bartsch; Douglas W. Shevlin; William S. Tung; Oliver Kisker; Samuel A. Wells Jr.; Paul J. Goodfellow

Publisher
John Wiley and Sons
Year
1995
Tongue
English
Weight
596 KB
Volume
14
Category
Article
ISSN
1045-2257

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✦ Synopsis

Abstract

The gene encoding the cell‐cycle regulatory protein p16, CDKN2, is localized on chromosome band 9p21. CDKN2 is frequently deleted or mutated in a variety of tumor cell lines, including pancreatic cancer cell lines and xenografts, as well as in some primary tumors. We examined 32 primary pancreatic adenocarcinomas for CDKN2 mutations and for loss of heterozygosity of 9p21 sequences to assess the role of CDKN2 in pancreatic carcinogenesis. Single‐strand conformation variant analysis (SSCV) and direct sequencing of the variants revealed somatic CDKN2 mutations in 11 of 32 tumors (five frame‐shift mutations, five nonsense mutations, and one missense mutation). One tumor appeared to be characterized by homozygous deletion of CDKN2. These results suggest that CDKN2 plays an important role during tumorigenesis or tumor progression in a significant proportion of pancreatic adenocarcinomas.

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