| Project/Area Number |
09557099
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 展開研究 |
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| Research Field |
Digestive surgery
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| Research Institution | HOKKAIDO UNIVERSITY |
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Principal Investigator |
KATOH Hiroyuki Fac.of Med., Hokkaido Univ., Pro., 医学部, 教授 (80002369)
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| Co-Investigator(Kenkyū-buntansha) |
TAKIMOTO Masato Fac.of Med., Hokkaido Univ., Lec., 医学部, 講師 (30179585)
KUZUMAKI Noboru Fac.of Med., Hokkaido Univ., Pro., 医学部, 教授 (80091445)
KONDO Satoshi Fac.of Med., Hokkaido Univ., Asso.Pro., 医学部, 助教授 (30215454)
高橋 利幸 北海道大学, 医学部, 講師 (40261284)
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| Project Period (FY) |
1997 – 1998
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| Project Status |
Completed (Fiscal Year 1998)
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| Budget Amount *help |
¥13,200,000 (Direct Cost: ¥13,200,000)
Fiscal Year 1998: ¥2,700,000 (Direct Cost: ¥2,700,000)
Fiscal Year 1997: ¥10,500,000 (Direct Cost: ¥10,500,000)
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| Keywords | Pancreatic Cancer / Cancer Gene Therapy / N116Y / Vector / 膵癌 / 遺伝子治療 / アデノウイルスペクター / RAS変異体 / CEAプロモーター |
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| Research Abstract |
The aim of this study is to assess whether N116Y can inhibit the proliferation of pancreatic cancer cell lines carrying K-ras mutations and cause reversion of the malignant phenotype. The growth inhibition activity of N116Y was evaluated by the colonyforming efficiency in selection medium. In order to examine the effect of N116Y on the neoplastic phenotype, we established N116Y-expressing clones and analyzed their growth ability in soft agar and tumorigenicity in nude mice. The growth of the eight pancreatic cancer cell lines was strongly inhibited by the transfection of pZIP-N116Y.Moreover, the N116Y-expressing clones became less spread and lost their anchorage-independent growth ability. Furthermore, they were nontumorigenic in vivo. N116Y significantly inhibits the growth of pancreatic cancer cell lines and causes reversion of the malignant phenotypes. These results suggest that N1I6Y may be a candidate gene for use in the gene therapy of pancreatic cancer.
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