Oncogenic mutations of RAC small GTPases in human cancers
Project/Area Number |
26430106
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Tumor biology
|
Research Institution | The University of Tokyo |
Principal Investigator |
Kawazu Masahito 東京大学, 大学院医学系研究科(医学部), 特任講師 (20401078)
|
Project Period (FY) |
2014-04-01 – 2017-03-31
|
Project Status |
Completed (Fiscal Year 2016)
|
Budget Amount *help |
¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2016: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2015: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2014: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
|
Keywords | がん遺伝子 / 乳がん / 低分子量GTP結合タンパク質 / 低分子量GTP結合蛋白質 |
Outline of Final Research Achievements |
We identified mutations in small GTPases in the genomes of triple negative breast cancers (TNBCs). These proteins were found to be oncogenic in a nude mice tumorigenic assay. The clonal analysis suggested that TP53 mutations and silencing of BRCA1 were earlier events during TNBC carcinogenesis, while mutations in small GTPases were considered to develop at later stage of tumor progression. Taken together, while, given its potent oncogenic capacity, mutations in GTPases is a potential therapeutic target, resistance may be acquired as a result of expansion of tumor clones without such mutations.
|
Report
(4 results)
Research Products
(2 results)
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[Journal Article] Transforming somatic mutations of mammalian target of rapamycin kinase in human cancer.2015
Author(s)
Yamaguchi H, Kawazu M, Yasuda T, Soda M, Ueno T, Kojima S, Yashiro M, Yoshino I, Ishikawa Y, Sai E, Mano H.
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Journal Title
Cancer Sci.
Volume: 106
Issue: 12
Pages: 1687-92
DOI
NAID
Related Report
Peer Reviewed / Open Access
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