1997 Fiscal Year Final Research Report Summary
Development of prophylactic agent against peritoneal carcinomatosis using S-DEX derivatives.
| Project/Area Number |
08457329
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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 | 一般 |
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| Research Field |
Digestive surgery
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| Research Institution | Kyoto Prefectural University of Medicine |
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Principal Investigator |
HAGIWARA Akeo Kyoto Prefectural University of Medicine. Surgery I,Lecturer., 医学部, 講師 (90198648)
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| Co-Investigator(Kenkyū-buntansha) |
SHIRASU Morio Kyoto Prefectural University of Medicine. Surgery I,Assistant., 医学部, 助手 (60275211)
TAKAHASHI Toshio Kyoto Prefectural University of Medicine. Surgery I,Professor., 医学部, 教授 (50079828)
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| Project Period (FY) |
1996 – 1997
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| Keywords | Cell adhesion / Cancer metastasis / Peritoneal Carcinomatosis / Prophylactic agent / Cell cycle / Apoptosis / Cell viability |
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| Research Abstract |
In the present research project, S-DEX was studies for (1) the effects on viability, cell cycle and cell adhesion of cancer cell lines using MMT assay, apoptosis-detecting kit and flow-cytometry in vitro and ex vivo, and (2) the prophylactic effect against peritoneal carcinomatosis using B-16 melanoma cell line. In in vitro and ex vivo examinations, incubation in medium containing 0.2% S-DEX significantly inhibited B-16 melanoma cells to adhere both to plastic wall and to the injured peritoneum, as compared to incubation in normal medium. In vitro examinations also showed that medium containing 0.2% S-DEX significantly increased the accumulation of cancer cell number in G1 phase, and that neither apoptosis nor necrosis was detected when the cells were turned into free state by medium containing 0.2% S-DEX.In vivo examination revealed that intraperitoneal administration of 0.2% of S-DEX (1ml/mouse) diminished the cancer cell number implanted into the injured peritoneum better than the intraperitoneal administration of S-DEX-free medium, and elongated the survival of mice with peritoneal carcinomatosis.
The above-mentioned results revealed that (1) S-DEX blocks the cell cycle at G1 phase, (2) S-DEX induces neither apoptosis nor necrosis, (3) S-DEX inhibits adhesion of cancer cells (4) S-DEX improves the survival of mice with peritoneal carcinomatosis. We concluded that S-DEX will become a prophylactic agent against peritoneal carcinomatosis.
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