| Budget Amount *help |
¥18,590,000 (Direct Cost: ¥14,300,000、Indirect Cost: ¥4,290,000)
Fiscal Year 2014: ¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2013: ¥8,320,000 (Direct Cost: ¥6,400,000、Indirect Cost: ¥1,920,000)
Fiscal Year 2012: ¥5,720,000 (Direct Cost: ¥4,400,000、Indirect Cost: ¥1,320,000)
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| Outline of Final Research Achievements |
Gastric gland mucins contain terminal α1,4-linked N-acetylglucosamine (αGlcNAc). This glycan prevents gastric cancer development by exhibiting antimicrobial activity against H. pylori as well as suppressing chronic inflammation. In this study, we analyzed expression of αGlcNAc and its pathological significance on human gastric diseases including gastric adenocarcinoma, pyloric gland adenoma, and chronic atrophic gastritis as well as Barrett's esophagus. Our results indicate that reduction or loss of αGlcNAc are associated with malignant potential of gastric differentiated-type adenocarcinoma and pyloric gland adenoma. We also showed that reduced αGlcNAc expression in chronic atrophic gastritis and Barrett's esophagus was a possible risk factor to develop gastric differentiated-type adenocarcinoma and Barrett's adenocarcinoma, respectively. In parallel, we generated new genetically engineered mice useful to study the regulatory roles of αGlcNAc in tumorigenesis of gastric cancer.
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