Budget Amount *help |
¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 1998: ¥600,000 (Direct Cost: ¥600,000)
Fiscal Year 1997: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 1996: ¥700,000 (Direct Cost: ¥700,000)
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Research Abstract |
In order to determine the genetic difference between superficial lesion and polypoid lesion, proliferation and apoptosis status and microsatellite instability status were examined using colorectal lesions with differing morphology. Proliferation and apoptosis status were examined in 37 colorectal adenomas with differing morphology by immunohistochmistry using anti-bc12 and anti-Ki67 antibodies. Materials were consisted of 11 polypoid adenomas, 16 flat elevated adenomas and 10 superficial adenomas, Proliferation status was similar among polypoid adenomas, flat elevated adenomas and superficial adenomas. However, concerning the relation between apoptosis status and morphology of the adenomas, superficial adenomas were tended to carry more active apoptosis status than polypoid adenomas. Microsatellite instability(MSI) was initially reported to be found in hereditary non polyposis colorectal cancer. Recently MSI is considered to be a marker to reflect DNA mismatch repair status and may refl
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ect the biological behavior. MSI were examined in 103 sporadic colorectal cancer in advanced stages. In this series, MSI was detected in 15.7% of sporadic colorectal cancers. Positive rate of MSI in colorectal cancers in the proximal colon and in the distal colon were 33% and 6%, respectively. MSI was found more in the proximal colon. Forty-four early colorectal cancers without family history of colorectal cancers were assayed for MSI status. Materials were consisted of 28 polypoid and 16 superficial lesions, and 19 lesions cited in the proximal colon and 25 lesions in the distal colon. MSI was positive in 11.4% of early colorectal cancers. In the proximal colon, superficial adenomas showed positive MSI more frequently than polypoid adenomas(44% vs 0%, p0.O4), which may suggest the different carcinogenesis between superficial lesions and polypoid lesions. The result in the present studies suggested that the carcinogenesis was different between in the proximal colon cancer and in the distal colorectal cancer. The tumorigenesis was also considered to be different between in the superficial lesions and in the polypoid lesions in the proximal colon by means of proliferation-apoptosis status and MSI status. Less
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