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Adverse prognosis of epigenetic inactivation in RUNX3 gene at 1p36 in human pancreatic cancer.

Authors: Nomoto, S  Kinoshita, T  Mori, T  Kato, K  Sugimoto, H  Kanazumi, N  Takeda, S  Nakao, A 
Citation: Nomoto S, etal., Br J Cancer. 2008 May 20;98(10):1690-5. Epub 2008 May 13.
Pubmed: (View Article at PubMed) PMID:18475302
DOI: Full-text: DOI:10.1038/sj.bjc.6604333

Alteration in transforming growth factor-beta signalling pathway is one of the main causes of pancreatic cancer. The human runt-related transcription factor 3 gene (RUNX3) is an important component of this pathway. RUNX3 locus 1p36 is commonly deleted in a variety of human cancers, including pancreatic cancer. Therefore, we examined genetic and epigenetic alterations of RUNX3 in human pancreatic cancer. Thirty-two patients with pancreatic cancer were investigated in this study. We examined the methylation status of RUNX3 promoter region, loss of heterozygosity (LOH) at 1p36, and conducted a mutation analysis. The results were compared with clinicopathological data. Promoter hypermethylation was detected in 20 (62.5%) of 32 pancreatic cancer tissues, confirmed by sequence of bisulphite-treated DNA. Loss of heterozygosity was detected in 11 (34.3%) of 32 pancreatic cancers. In comparison with clinicopathological data, hypermethylation showed a relation with a worse prognosis (P=0.0143). Hypermethylation and LOH appear to be common mechanisms for inactivation of RUNX3 in pancreatic cancer. Therefore, RUNX3 may be an important tumour suppressor gene related to pancreatic cancer.


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CRRD Object Information
CRRD ID: 2324956
Created: 2010-05-17
Species: All species
Last Modified: 2010-05-17
Status: ACTIVE


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