Project/Area Number |
26640108
|
Research Category |
Grant-in-Aid for Challenging Exploratory Research
|
Allocation Type | Multi-year Fund |
Research Field |
Tumor therapeutics
|
Research Institution | Japanese Foundation for Cancer Research |
Principal Investigator |
Fujita Naoya 公益財団法人がん研究会, がん化学療法センター, 所長 (20280951)
|
Research Collaborator |
TAKEMOTO Ai
SATO Shigeo
TAKAGI Satoshi
TAKAMI Miho
SEKIGUCHI Takaya
MIYATA Kenichi
TAKATORI Kazuki
|
Project Period (FY) |
2014-04-01 – 2016-03-31
|
Project Status |
Completed (Fiscal Year 2015)
|
Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2015: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2014: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
|
Keywords | 癌 / 分子標的治療 / 血小板 |
Outline of Final Research Achievements |
Platelets are well known to be associated with tumor growth and metastasis. We previously obtained unexpected results that platelet depletion by an anti-mouse platelet antibody (anti-GPIbalpha antibody) led to the increase in xenografted tumor volume. Thus, we tried to clarify the molecular mechanisms underlying platelet depletion-mediated tumor growth. We firstly performed cDNA microarray using mRNA samples from xenografted tumors that had been treated with an anti-GPIbalpha antibody or a control antibody. We could not find out any candidate genes. Immunohistochemical analysis revealed that platelet depletion induced angiogenesis without changing plasma PDGF concentration. Rather, platelet depletion resulted in the decrease in plasma PDGF concentration. Since the used anti-platelet antibody exhibited platelet aggregation-inducing ability, the antibody might promote in vivo tumor growth by enhancing the secretion of some growth factors from platelets.
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