Project/Area Number |
13470230
|
Research Category |
Grant-in-Aid for Scientific Research (B)
|
Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
General surgery
|
Research Institution | HOKKAIDO UNIVERSITY |
Principal Investigator |
KONDO Satoshi Hokkaido University Graduate of School of Med, Asso. Prof., 大学院・医学研究科, 助教授 (30215454)
|
Co-Investigator(Kenkyū-buntansha) |
MORIUCHI Tetsuya Hokkaido University, Institute For Genetic Medicine, Prof, 遺伝子病制御研究所, 教授 (20174394)
TADA Mitsuhiro Hokkaido University, Institute For Genetic Medicine, Asso, Prof, 遺伝子病制御研究所, 助教授 (10241316)
KATOH Hiroyuki Hokkaido University Graduate of School of Med, Prof, 大学院・医学研究科, 教授 (80002369)
|
Project Period (FY) |
2001 – 2002
|
Project Status |
Completed (Fiscal Year 2002)
|
Budget Amount *help |
¥14,000,000 (Direct Cost: ¥14,000,000)
Fiscal Year 2002: ¥2,500,000 (Direct Cost: ¥2,500,000)
Fiscal Year 2001: ¥11,500,000 (Direct Cost: ¥11,500,000)
|
Keywords | cancer gene therapy / specific promotor / adenoviralvector / RCAS1 / Caveolin-1 / SCCA / IRRES / 癌 / SCCA2 / hTERT / 遺伝子治療 |
Research Abstract |
We studied the cancer specific antigens expressed in the several organ tumors. In pancreatic cancer, 90% were positive for RCAS1 gene. Moreover, overexpression of RCAS1 gene was correlated with the prognosis of patients with pancreatic cancer, extrahepatic bile duct carcinoma and esophageal cancer. Caveolin-1 expression was also correlated with with the prognosis of patients with pancreatic cancer. We made a replication-deficient recombinant KLAKLAK2 or Bax adenovirus driven by the RCAS1promoter (Ad RCAS1-KLAKLAK2, Ad RCAS1-Bax) or the SCCA promoter (Ad SCCA-KLAKLAK2). We demonstrated that the expression of KLAKLAK2 and growth inhibition were all specific to the cancer cell lines that were SCCA positive, whereas no growth retardation was observed in human normal cell lines after Ad SCCA-KLAKLAK2 infection.
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