| Project/Area Number |
16590052
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Biological pharmacy
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| Research Institution | Nagasaki University |
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Principal Investigator |
OZAKI Keiichi Nagasaki University, Graduate School of Biomedical Sciences, Associate professor, 大学院・医歯薬学総合研究科, 助教授 (50252466)
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| Project Period (FY) |
2004 – 2005
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| Project Status |
Completed (Fiscal Year 2005)
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| Budget Amount *help |
¥3,600,000 (Direct Cost: ¥3,600,000)
Fiscal Year 2005: ¥1,200,000 (Direct Cost: ¥1,200,000)
Fiscal Year 2004: ¥2,400,000 (Direct Cost: ¥2,400,000)
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| Keywords | EGF receptor / Sprouty / ERK / Gefitinib / lung cancer / Akt / PI3 kinase / MEK inhibitor / MAP kinase / PI3-kinase / tyrosine kinase |
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| Research Abstract |
1,Relationship between the sensitivity to Gefitinib and two Sprouty-2 transcripts in tumor cells
Sensitivity to Iressa (gefitinib) in human lung cancers was found to be related with expression pattern of two transcripts of human Sprouty-2 genes (long and short forms, respectively). The tumors expressing only short forms of Sprouty-2 transcripts were resistant to Iressa, whereas the cells with long forms were sensitive. The Sprouty-2 transcripts may be a new biomarker for determining the sensitivity to Iressa in tumors.
2,New strategies against Gefitinib (Iressa)-resistant tumor cells
1)The combination of MEK inhibitors and HDAC inhibitors provides an efficient chemotherapeutic strategy for the treatment of tumor cells in which the ERK pathway is constitutively activated.
2)The combination of a PI3 kinase/Akt pathway inhibitor and doxorubicin provides an efficient chemotherapeutic strategy for the treatment of tumor cells in which the PI3 kinase/Akt pathway is constitutively activated and the p53 pathway is functional.
These combination therapies may be a new strategy for overcoming Iressa-resistance in tumors.
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