| Project/Area Number |
61570651
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Digestive surgery
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| Research Institution | Osaka University Medical School |
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Principal Investigator |
MONDEN Takushi Osaka University Medical School, 医学部, 助手 (20174477)
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| Co-Investigator(Kenkyū-buntansha) |
MORIMOTO Hideki Osaka University Hospital, 医学部附属病院, 医員
OUKDA Hiroshi Osaka University Medical School, 医学部, 講師 (40028577)
SHIMANO Takashi Osaka University Medical School, 医学部, 助手 (80144476)
森本 秀起 大阪大学, 医学部附属病院(外科学), 医員
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| Project Period (FY) |
1986 – 1987
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| Project Status |
Completed (Fiscal Year 1987)
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| Budget Amount *help |
¥2,200,000 (Direct Cost: ¥2,200,000)
Fiscal Year 1987: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 1986: ¥1,400,000 (Direct Cost: ¥1,400,000)
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| Keywords | Colorectal cancer / Colorectal adenoma / Oncogene mRNA / Northern blot analysis / histo-in situ hybridzation / HISTO-IN SITU HYBRIDIZATION / mRNA / 大腸前癌病変 / 転写活性 / スルホン化DNAプローブ / 癌遺伝子 |
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| Research Abstract |
By immunohistological technique using a monoclonal antibody against carcinoembryonic antigen and antisera against two types of gastrointestinal mucus antigens, we have collected 39 cases of colorectal cancer and 20 cases of adenoma which expressed fetal phenotype in nature.
Histo-in situ hybridization on these carcinomas and adenomas utilizing sulfonated probes of v-Ha-ras(880bp) and v-myc(990bp) oncogenes revealed that 28%(11/39) and 41%(16/39) of carcinomas showed accelerated transcription of Ha-ras and c-myc respectively. The results of in situ hybridization and Northern blot analysis agreed well in most cases.
In contrast, many of the colorectal adenomas did not show the accelerated transcription of the oncogenes, and only a few adenomas were hybridized weakly by either probe of sulfonated v-Ha-ras or v-myc.
The tissue culture of the adenomas was successful for about 3 months and some of the cultured adenomas showed a high atypism in morphology.
These data may indicate the possibility of malignant transformation of such adenomas that have fetal phenotype as well as accelerated transcription rate of oncogenes.
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