| Budget Amount *help |
¥2,990,000 (Direct Cost: ¥2,300,000、Indirect Cost: ¥690,000)
Fiscal Year 2016: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2015: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
|
|---|
| Outline of Final Research Achievements |
The CGH analysis has shown that FGF9, MAP3K10, and AKT2 genes can be related to the resistance to EGFR inhibitors. Using overexpressing cell lines, the resistance has been demonstrated in FGF9 and AKT2 genes, which can be cancelled by FGFR and PI3K inhibitors, respectively, but not in MAP3K10 gene.
In clinical samples, FGF9 amplification was observed at a frequency of 8/145 (5.5%) and tended to be related to wild-type KRAS (7/96, 7.3%). Furthermore, FGF9 amplification was not observed in any of the samples from the 15 responders to anti-EGFR therapies but was observed in one sample from the seven non-responders with wild-type KRAS. In addition, the difference was not significant, pancreatic cancer patients with high levels of Akt2 expression tended to have a poorer response and a shorter progression-free survival period after treatment with an EGFR inhibitor than those with low expression levels.
|
