1994 Fiscal Year Final Research Report Summary
Allelic Loss of Chromosome 16 q and Reduced Expression of E-cadherin during Progression and Metastasis of Ovarian Cancer
Project/Area Number |
05671374
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Research Category |
Grant-in-Aid for General Scientific Research (C)
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Allocation Type | Single-year Grants |
Research Field |
Obstetrics and gynecology
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Research Institution | Ehime University |
Principal Investigator |
KIHARA Tshimasa Ehime Univ.School of Medicine, instructor, 医学部, 助手 (90234327)
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Project Period (FY) |
1993 – 1994
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Keywords | E-cadherin / Chromosome 16q / LOH / ovarian cancer / endometrial cancer / tumor suppressor gene / microsatellite / immunohistochemistry |
Research Abstract |
Allelic loss on chromosomal region, 16q22.1, harboring E-cadherin have been demonstrated in prostate, breast, and hepatocellular carcinomas. We investigated allelic loss of chromosome 16q and expression of E-cadherin in ovarian and endometrial cancers in order to reveal the suppressive role of E-cadherin to tumor progression. Paired normal and tumor tissue DNAs were extracted from 26 cases with ovarian cancer and 50 cases with endometrial cancer, and analyzed loss of heterozygosity (LOH) of chromosome 16q. Tissue sections from 15 cases of ovarian cancer and 15 cases of endometrial cancer were immunohistochemically examined for expression of the E-cadherin. LOH of chromosome 16q was detected in 15 (58%) of 26 ovarian cancers, and in 21 (42%) of 50 endometrial cancers. Most cases of ovarian cancer showing LOH were advanced stage. In endometrial cancer, LOH was significantly correlated with histological grade, and the patients' survival. Immunohistochemical staining pattern of E-cadherin was classified as absent, heterogenous, and homogenous staining on cell to cell border. Absent and heterogenous staining were considered as reduced expression of E-cadherin with comparison of staining on normal tissue. Reduced expression of the E-cadherin was observed 60% (9/15) in ovarian cancer, and 27% (4/15) in endometrial cancer. Reduced expression of the E-cadherin was associated with LOH of chromosome 16q, although not significant. These results indicate that reduced expression of the E-cadherin and LOH of chromesome 16q were associated with tumor progression.
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