Project/Area Number |
23591005
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Gastroenterology
|
Research Institution | Research Institute, International Medical Center of Japan |
Principal Investigator |
MURATA Kazumoto 独立行政法人国立国際医療研究センター, その他部局等, その他 (40345971)
|
Co-Investigator(Kenkyū-buntansha) |
IMAMURA Masatoshi 国立国際医療研究センター, 国府台病院, 医長 (60445129)
|
Project Period (FY) |
2011 – 2013
|
Project Status |
Completed (Fiscal Year 2013)
|
Budget Amount *help |
¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2013: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2012: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2011: ¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
|
Keywords | 肝癌 / 腫瘍マーカー / PIVKA-II / EMT |
Research Abstract |
PIVKA-II is generally used in hepatocellular carcinoma (HCC) clinic, but precise mechanism of PIVKA-II production is still unkown. We have demonstrated that PIVKA-II was produced when HCC became metastatic phenotype (epithelial mesenchymal transition: EMT) that was impaired uptake of vitamin K by actin rearrangement. In this project, we demonstrated that further EMT caused impairment of liver specific protein synthesis, resulting in impairment of PIVKA-II production even though HCC still grew. Moreover, findings in enhanced ultrasonography well-correlated with PIVKA-II production in surgically resected HCC. Taken together, PIVKA-II could be an biological marker for HCC as well as a tumor marker of HCC.
|