2012 Fiscal Year Final Research Report
Elucidation of the mechanisms involved in development and suppression ofBarrett's esophagus: Results of joint Japan-U.S. research
| Project/Area Number |
22590692
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Gastroenterology
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| Research Institution | Hyogo Medical University |
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Principal Investigator |
WATARI Jiro 兵庫医科大学, 医学部, 教授 (10311531)
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| Co-Investigator(Kenkyū-buntansha) |
MIWA Hiroto 兵庫医科大学, 医学部, 教授 (80190833)
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| Project Period (FY) |
2010 – 2012
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| Keywords | 上部消化管学(食道,胃,十二指腸) |
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| Research Abstract |
We evaluated several molecular alterations including microsatellite instability (MSI); the CpG island methylation status of hMLH1, p16, E-cadherin and APC genes; and monoclonal antibody Das-1, which specifically reacts with BE in specialized intestinal metaplasia (SIM), as well as in columnar lined epithelium (CLE) without SIM in BE mucosa. Additionally, we investigated changes in the above molecular markers in a randomized control trial, comparing PPI administration versus PPI non-administration groups. Our results showed no significant differences in the frequency of MSI, or methylation at any genes investigated in SIM or CLE. In contrast, Das-1 reactivity was significantly higher in SIM versus CLE. The frequency of methylation and Das-1 reactivity among Japanese was similar to that of BE in the U.S. population, a finding which corroborates previous reports. In patients administered PPI, MSI and hypermethylation at p16, E-cadherin, and APC genes disappeared following interventon, while patients without PPI did not show this tendency. These results indicate that CLE may be a precancerous lesion as well as SIM, and there is no difference in the molecular characteristics of BE between Japanese and U.S. populations. Furthermore, PPI may promote regression of the molecular alterations involved in BE.
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