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

Authors: Nozawa, H  Oda, E  Ueda, S  Tamura, G  Maesawa, C  Muto, T  Taniguchi, T  Tanaka, N 
Citation: Nozawa H, etal., Int J Cancer. 1998 Aug 12;77(4):522-7.
Pubmed: (View Article at PubMed) PMID:9679752

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.


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CRRD Object Information
CRRD ID: 1600013
Created: 2007-02-26
Species: All species
Last Modified: 2007-02-26
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.