✦ LIBER ✦

Functionally inactivating point mutation in the tumor-suppressor IRF-1 gene identified in human gastric cancer

✍ Scribed by Hiroaki Nozawa; Eri Oda; Seiji Ueda; Gen Tamura; Chihaya Maesawa; Tetsuichiro Muto; Tadatsugu Taniguchi; Nobuyuki Tanaka

Publisher: John Wiley and Sons
Year: 1998
Tongue: French
Weight: 155 KB
Volume: 77
Category: Article
ISSN: 0020-7136
DOI: 10.1002/(sici)1097-0215(19980812)77:4<522::aid-ijc8>3.0.co;2-w

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✦ Synopsis

Loss of heterozygosity (LOH) observed in human tumors strongly suggests the existence of (a) tumor-suppressor gene(s) at the concerned locus. A series of studies has revealed that LOH on the long arm of chromosome 5 (5q) frequently occurs in differentiated gastric adenocarcinomas. Furthermore, it has been shown that the interferon regulatory factor-1 (IRF-1) locus on chromosome 5q31.1 is one of the common minimal regions of LOH in these cancers. IRF-1 is a transcriptional activator that shows tumor-suppressor activity in the mouse. In the present study, we examined the sequence of the IRF-1 gene in 9 cases of histologically differentiated gastric adenocarcinomas, all of which exhibited LOH at the IRF-1 locus. We identified a mis-sense mutation in the residual allele in one case. This mutated form of IRF-1 showed markedly reduced transcriptional activity. In addition, overexpression of wild-type IRF-1 induced cell-cycle arrest, whereas such activity was attenuated in the mutant IRF-1. These results suggest that the loss of functional IRF-1 is critical for the development of human gastric cancers. Int.

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