Early drivers of gastric cancer

August 9, 2017 by Leigh Macmillan, Vanderbilt University

Gastric cancer – a leading cause of cancer-related deaths worldwide – is commonly diagnosed at a late stage when most patients have a poor prognosis.

Wael El-Rifai, M.D., Ph.D., and colleagues are exploring the molecular alterations that drive gastric carcinogenesis, to improve early detection, treatment and prevention. They previously showed that knocking out (eliminating) the gene Tff1 in mice induces that include low- and high-grade dysplasia and adenocarcinomas.

Now, they have investigated in low-grade dysplastic lesions and normal stomach tissue from mice and in gastric cancer and normal stomach tissue from humans. Using bioinformatics approaches, they identified transcription (gene expression) networks that were consistently deregulated in both mouse and human lesions.

The findings, reported in the July issue of Genes, Chromosomes and Cancer, suggest that activation of MYC, STAT3, and beta-catenin transcription networks could be an early molecular step in gastric tumorigenesis. The findings also support using the Tff1-knockout mouse model for in vivo studies of molecular mechanisms in .

Explore further: First roadmap of stomach cancer super-enhancers paves the way for new treatments

More information: Zheng Chen et al. Integrated expression analysis identifies transcription networks in mouse and human gastric neoplasia, Genes, Chromosomes and Cancer (2017). DOI: 10.1002/gcc.22456

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