Project/Area Number |
06671243
|
Research Category |
Grant-in-Aid for General Scientific Research (C)
|
Allocation Type | Single-year Grants |
Research Field |
Digestive surgery
|
Research Institution | CHIBA UNIVERSITY SCHOOL OF MEDICINE |
Principal Investigator |
KOBAYASHI Susumu CHIBA UNIVERSITY SCHOOL OF MEDICINE ASSISTANT, 医学部, 助手 (50234828)
|
Co-Investigator(Kenkyū-buntansha) |
IMAZEKI Hideo CHIBA UNIVERSITY SCHOOL OF MEDICINE ASSISTANT, 医学部付属病院, 助手 (60272308)
ISONO Kaichi CHIBA UNIVERSITY SCHOOL OF MEDICINE PROFESSOR, 医学部, 教授 (70009489)
遠藤 正人 千葉大学, 医学部附属病院, 医員
|
Project Period (FY) |
1994 – 1995
|
Project Status |
Completed (Fiscal Year 1995)
|
Budget Amount *help |
¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 1995: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1994: ¥500,000 (Direct Cost: ¥500,000)
|
Keywords | c-myc / colorectal cancer / antisense oligo DNA / CIP1 / WAF1 / Northern blot hybridization / C‐myc |
Research Abstract |
Northern blot hybridization revealed messenger RNA overexpression of c-myc gene in 85% colorectal carcinoma tissues, however, there was no overexpression for max gene. In our investigation, the antisense DNA for the translation starting locus could not depress cell growth of COLO-320 DM which derived from human colorectal cancer and had c-myc mRNA overexpression. Thereafter, we investigated the mRNA expression of CIP1/WAF1 gene which was cycline dependent kinase (CDK) inhibitor in colorectal carcinoma to detect more important cell growth genes. The expression in tumor tissues were depressed in all 16 case compared with the correspondent nontumor tissues. We also detect the p53 gene mutation through the PCR-SSCP method for the correpondent DNA.We could identified 6 mutation cases in 16 cases. These mutant cases indicated the more depressed mRNA expression compared with wilds p53 cases. These result indicated that there could be the possibility for more useful therapy through CIP1/WAF1 gene control
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