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A basic research of p73 activation as a novel treatment for p53-mutant type cancer

Research Project

Project/Area Number 26460624
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Research Field Applied pharmacology
Research InstitutionUniversity of Tsukuba

Principal Investigator

HYODO Ichinosuke  筑波大学, 医学医療系, 教授 (60416469)

Co-Investigator(Kenkyū-buntansha) 遠藤 慎治  筑波大学, 医学医療系, 講師 (40625919)
大和 建嗣  筑波大学, 医学医療系, 研究員 (50174751)
山本 祥之  筑波大学, 附属病院, 病院講師 (00649288)
Project Period (FY) 2014-04-01 – 2017-03-31
Project Status Completed (Fiscal Year 2016)
Budget Amount *help
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2016: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2015: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2014: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Keywordsp73 / がん / p73活性化 / ΔNp73 / iASPP / TP53変異細胞 / MDM2
Outline of Final Research Achievements

p73 has a high homology to tumor-suppressor gene p53, and acts as a translational factor like p53 in p53-mutant type cancer cells.
In this study, we evaluated the tumor growth inhibition of p73 in human tumor cell lines. p73 was induced by 5-FU or irinotecan administration in the colon cancer cells (DLD-1, HCT116). Using HCT116, the function of p73 was investigated with various inhibition of related-molecules under 5-FU exposure. As the results, p73 tumor-suppressive function was little in this cancer line regardless of harboring p53 mutation. Further studies are needed to develop a novel strategy using p73 for anticancer treatments.

Report

(4 results)
  • 2016 Annual Research Report   Final Research Report ( PDF )
  • 2015 Research-status Report
  • 2014 Research-status Report

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Published: 2014-04-04   Modified: 2018-03-22  

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