2015 Fiscal Year Final Research Report
JAK-STAT inhibitor as a new drug for treatment of anaplastic thyroid cancer
| Project/Area Number |
25461998
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Multi-year Fund |
|---|
| Section | 一般 |
|---|
| Research Field |
General surgery
|
|---|
| Research Institution | Tokyo Medical University |
|---|
Principal Investigator |
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
FUJIMORI Minoru 東京医科大学, 医学部, 兼任教授 (00262725)
|
|---|
| Project Period (FY) |
2013-04-01 – 2016-03-31
|
| 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 |
|---|
| 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.
|
| Free Research Field |
外科腫瘍学
|
