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논문 기본 정보

자료유형
학술저널
저자정보
Junsik Kwon (분당 서울대병원) Ju-Hee Lee (분당 서울대병원) Ye Seob Jee (단국대학교병원) Do-Jung Park (분당 서울대병원) Hyung-Ho Kim (분당 서울대병원) Hyuk-Joon Lee (서울대학교) Han-Kwang Yang (서울대학교) Kuhn Uk Lee (서울대학교) Hye Seung Lee (분당 서울대병원)
저널정보
대한외과학회 Annals of Surgical Treatment and Research 대한외과학회지 Vol.79 No.2
발행연도
2010.8
수록면
94 - 102 (9page)

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Purpose: Mutated p53 is a tumor suppressor gene, hMLH1 is a mismatch repair gene, and hypermethylation of hMLH1 follows microsatellite instability (MSI). This research’s aim is to investigate mutated p53, inactivated hMLH1 and MSI in gastric cancer and their clinicopathologic implications.
Methods: Between 2003 and 2007, 618 patients underwent curative radical gastrectomy for gastric cancer at Seoul National University Bundang Hospital in Korea. We reviewed their medical charts and the pathologic reports with immunohistochemistry for p53, hMLH1 and polymerase chain reaction for MSI in 509, 499, and 561 cases, respectively. These genetic markers were statistically compared with clinicopathologic features and postoperative survival.
Results: The expression ratios of mutated p53, inactivated hMLH1, and MSI were 32.8%, 8.4%, and 8.7%, respectively. Mutation of p53 occurred more frequently in aged group (over 40), differentiated group (against the non-differentiated group), intestinal type, infiltrative type and positive lymph node metastasis group. Inactivated hMLH1 occurred more frequently in aged group, differentiated group, intestinal type and expanding growth type group. MSI was found more frequently in aged group, intestinal type and expanding growth type group. All three genetic markers had no significant associations with the 5-year survival.
Conclusion: We identified significant relationships between mutated p53, inactivated hMLH1, and MSI with some clinicopathologic features of gastric cancer. However, there were no apparent relationships between p53, hMLH1, and MSI and prognosis.

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INTRODUCTION
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