| Project/Area Number |
26893039
|
|---|
| Research Category |
Grant-in-Aid for Research Activity Start-up
|
| Allocation Type | Single-year Grants |
|---|
| Research Field |
Surgical dentistry
|
|---|
| Research Institution | Chiba University |
|---|
Principal Investigator |
NAKASHIMA DAI 千葉大学, 医学(系)研究科(研究院), 助教 (50431747)
|
|---|
| Project Period (FY) |
2014-08-29 – 2016-03-31
|
| Project Status |
Completed (Fiscal Year 2015)
|
| Budget Amount *help |
¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
Fiscal Year 2015: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2014: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
|
|---|
| Keywords | Decorin / 口腔扁上皮癌 / S-1 / AKT経路 / 口腔扁平上皮癌 / AKT 経路 / 術前補助的化学療法 |
|---|
| Outline of Final Research Achievements |
Our previous study suggested that decorin (DCN) silencing cells increase chemosusceptibility to S-1, consisted of tegafur, prodrug of 5-fluorouracil, however, detail mechanism of DCN for chemotherapy is still unknown. In this study, we demonstrated decreasing cell proliferation and increasing apoptosis with dephosphorylation of AKT after S-1 chemotherapy in vitro and in vivo. We then investigated whether DCN expression predicts the clinical responses of neoadjuvant chemotherapy (NAC) using S-1 (S-1 NAC) for oral cancer patients. Interestingly, low DCN expression was observed in 5 of 6 cases with complete responses to S-1 NAC, and in one case of 10 cases with stable/progressive disease, indicating that S-1 chemosensitivity is dramatically effective in oral cancer patients with low DCN expression compared with high expression. Our findings suggest that DCN is a key regulator for chemoresistant mechanisms, and is a predictive immunomarker of the response to S-1 NAC and patient prognosis.
|
