JAK-STAT inhibitor as a new drug for treatment of anaplastic thyroid cancer
| Project/Area Number |
25461998
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
General surgery
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| Research Institution | Tokyo Medical University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
FUJIMORI Minoru 東京医科大学, 医学部, 兼任教授 (00262725)
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2015: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000)
Fiscal Year 2014: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2013: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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| Keywords | 甲状腺未分化癌 / JAK-STAT経路 / パクリタキセル感受性・耐性 / JAK阻害剤 / 新規治療 / 標的治療 |
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| Outline of Final Research Achievements |
Differences in cDNA microarray gene expression profiles before and after treatment with paclitaxel were analyzed in two ATC cell lines: KTA-3 cells, which are sensitive to paclitaxel, and TTA-2 cells, which are resistant to paclitaxel. Genes in the JAK-STAT pathway (KEGG classification) were downregulated significantly in KTA-3 cells compared with TTA-2 cells after treatment with paclitaxel. PAGE showed that BRCA1-related genes including JAK1, JAK2 and STAT3 were downregulated most significantly in KTA-3 cells compared with TTA-2 cells after paclitaxel treatment. Several JAK inhibitors inhibited cell growth in paclitaxel-resistant ATC cells. Also IL-6 was reduced by paclitaxel in KTA-3 cells and JAK inhibitors in both cells. JAK inhibitors may be new drugs for treatment of paclitaxel resistant ATC. IL-6 may be a potential biomarker for treatment of JAK inhibitors.
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Report
(4 results)
Research Products
(19 results)
