| Project/Area Number |
13670800
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Single-year Grants |
|---|
| Section | 一般 |
|---|
| Research Field |
Pediatrics
|
|---|
| Research Institution | KYOTO UNIVERSITY |
|---|
Principal Investigator |
ADACHI Souichi Kyoto University, Graduate school of medicine, Instructor, 医学研究科, 助手 (10273450)
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
LIN Ying-wei Kyoto University, Graduate school of medicine, Instructor, 医学研究科, 助手 (40283600)
NAKAHATA Tatsutoshi Kyoto University, Graduate school of medicine, Professor, 医学研究科, 教授 (20110744)
|
|---|
| Project Period (FY) |
2001 – 2002
|
| Project Status |
Completed (Fiscal Year 2002)
|
| Budget Amount *help |
¥3,000,000 (Direct Cost: ¥3,000,000)
Fiscal Year 2002: ¥1,500,000 (Direct Cost: ¥1,500,000)
Fiscal Year 2001: ¥1,500,000 (Direct Cost: ¥1,500,000)
|
|---|
| Keywords | NSAID / Apoptosis / Mitochondria / Anti-tumor effect / CLL / Neuroblastoma / CLL / カスパーゼ / 慢性リンパ性白血病 |
|---|
| Research Abstract |
We have been reported that etodolac, a chiral non-steroidal anti-inflammatory drug (NSAID) was shown to be pro-apoptotic in primary CLL cells both in vitro and in vivo. Here we also show anti-tumor effect of both the R and S-enatiomers of etodolac against several cancers including neuroblastoma cell line and primary CML cells. Etodolac has additive cytotoxic effects from combinations with other chemotherapeutic drugs such as cyclophosphamide and vincristine. The mechanism of cell death is mitochondrial-dependent pathway because we show that (1) dysfunction of mitochondrial oxygen uptake and membrane potential (2) activation of caspase 9 and caspase 3 (3) degradation of Mcl-1
|
