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Novel strategies for endogenous danger signals by a TLR7 aptamer

Research Project

Project/Area Number 25462049
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Research Field Digestive surgery
Research InstitutionNagoya University

Principal Investigator

Uehara Keisuke  名古屋大学, 医学部附属病院, 病院講師 (50467320)

Co-Investigator(Kenkyū-buntansha) NAGINO MASATO  名古屋大学, 医学系研究科, 教授 (20237564)
YOKOYAMA YUKIHIRO  名古屋大学, 医学部附属病院, 講師 (80378091)
KOKURYO TOSHIO  名古屋大学, 医学系研究科, 特任講師 (60378023)
YOSHIOKA YUICHIRO  名古屋大学, 医学部附属病院, 助教 (50597854)
Project Period (FY) 2013-04-01 – 2016-03-31
Project Status Completed (Fiscal Year 2015)
Budget Amount *help
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2015: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2014: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2013: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
KeywordsDenger Signal / Danger signal
Outline of Final Research Achievements

We analyzed the expression of TLR7 and other members of the TLR family, including TLR3, TLR4, TLR5, TLR6 and TLR9, and the clinicopathological features of cholangiocarcinoma and pancreatic cancer. TLR7 was highly expressed in both cancers. In addition, TLR3, TLR4, TLR5 and TLR6 were highly expressed in both cancers.
Administration of a TLR7 agonist suppressed cell proliferation in a cholangiocarcinoma cell line and a pancreatic cancer cell line. Furthermore, a TLR7 agonist demonstrated anti-cancer effects in a xenograft mouse model. This study suggests that novel anti-cancer therapies can be developed to target TLR7.

Report

(3 results)
  • 2015 Annual Research Report   Final Research Report ( PDF )
  • 2013 Research-status Report

URL: 

Published: 2014-07-25   Modified: 2019-07-29  

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