Elucidating clinical significance of CYLD down-regulation for establishing individualized cancer therapy
| Project/Area Number |
26713006
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| Research Category |
Grant-in-Aid for Young Scientists (A)
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| Allocation Type | Partial Multi-year Fund |
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| Research Field |
Medical pharmacy
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| Research Institution | Kumamoto University |
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Principal Investigator |
Jono Hirofumi 熊本大学, 医学部附属病院, 准教授 (40515483)
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| Project Period (FY) |
2014-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥18,980,000 (Direct Cost: ¥14,600,000、Indirect Cost: ¥4,380,000)
Fiscal Year 2017: ¥3,510,000 (Direct Cost: ¥2,700,000、Indirect Cost: ¥810,000)
Fiscal Year 2016: ¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2015: ¥5,590,000 (Direct Cost: ¥4,300,000、Indirect Cost: ¥1,290,000)
Fiscal Year 2014: ¥6,110,000 (Direct Cost: ¥4,700,000、Indirect Cost: ¥1,410,000)
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| Keywords | 個別医療 / 予後予測因子 / シグナル伝達 / 薬剤感受性 / 分子標的薬 / 癌 |
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| Outline of Final Research Achievements |
The purpose of our study was to elucidate the clinical significance of tumor suppressor CYLD down-regulation in cancer patient with poor prognosis. In this study, we revealed as follows: 1. CYLD down-regulation in tumor tissues was caused by multiple factors, such as hypoxic environment and microenvironment of the tumor. 2. Some of cell signal transduction, such as TGF-β, NF-kB, and MAPK signaling may be involved in tumor malignancy caused by CYLD down-regulation. 3. Molecular diagnosis targeted CYLD expression may be useful for predicting the effect of anticancer agents. Those results reveled the molecular function of CYLD in tumor tissues, and may open up novel strategies for establishing personalized medicine for malignant tumors.
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Report
(5 results)
Research Products
(32 results)
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[Journal Article] Loss of CYLD promotes cell invasion via ALK5 stabilization in oral squamous cell carcinoma2018
Author(s)
Shinriki S, Jono H, Maeshiro M, Nakamura T, Guo J, Li JD, Ueda M, Yoshida R, Shinohara M, Nakayama H, Matsui H, Ando Y.
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Journal Title
Journal of Pathology
Volume: 244
Issue: 3
Pages: 367-379
DOI
Related Report
Peer Reviewed / Int'l Joint Research
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[Journal Article] An oncofetal antigen, IMP-3-derived long peptides induce immune responses of both helper T cells and CTLs.2016
Author(s)
Hirayama M, Tomita Y, Yuno A, Tsukamoto H, Senju S, Imamura Y, Sayem MA, Irie A, Yoshitake Y, Fukuma D, Shinohara M, Hamada A, Jono H, Yuba E, Kono K, Yoshida K, Tsunoda T, Nakayama H, Nishimura Y
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Journal Title
Related Report
Peer Reviewed
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[Journal Article] Intrinsic TGF-β2-triggered SDF-1-CXCR4 signaling axis is crucial for drug resistance and a slow-cycling state in bone marrow-disseminated tumor cells.2015
Author(s)
Nakamura T, Shinriki S, Jono H, Guo J, Ueda M, Hayashi M, Yamashita S, Zijlstra A, Nakayama H, Hiraki A, Shinohara M, Ando Y.
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Journal Title
Oncotarget
Volume: 6
Pages: 1008-1019
Related Report
Peer Reviewed / Open Access / Acknowledgement Compliant
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[Journal Article] Osteopontin-integrin α(v)β(3) axis is crucial for 5-fluorouracil resistance in oral squamous cell carcinoma.2015
Author(s)
Nakamura T, Shinriki S, Jono H, Ueda M, Nagata M, Guo J, Hayashi M, Yoshida R, Ota T, Ota K, Kawahara K, Nakagawa Y, Yamashita S, Nakayama H, Hiraki A, Shinohara M, Ando Y.
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Journal Title
FEBS Lett
Volume: 589
Issue: 2
Pages: 231-239
DOI
Related Report
Peer Reviewed / Open Access
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[Journal Article] Hypoxia suppresses cylindromatosis (CYLD) expression to promote inflammation in glioblastoma: possible link to acquired resistance to anti-VEGF therapy.2014
Author(s)
Guo J, Shinriki S, Su Y, Nakamura T, Hayashi M, Tsuda Y, Murakami Y, Tasaki M, Hide T, Takezaki T, Kuratsu J, Yamashita S, Ueda M, Li JD, Ando Y, Jono H.
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Journal Title
Oncotarget
Volume: 5
Pages: 6353-6364
Related Report
Peer Reviewed / Open Access
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[Journal Article] Clinical significance of CYLD downregulation in breast cancer.2014
Author(s)
Hayashi M, Jono H, Shinriki S, Nakamura T, Guo J, Sueta A, Tomiguchi M, Fujiwara S, Yamamoto-Ibusuki M, Murakami K, Yamashita S, Yamamoto Y, Li JD, Iwase H, Ando Y.
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Journal Title
Breast Cancer Res Treat.
Volume: 143
Issue: 3
Pages: 447-457
DOI
Related Report
Peer Reviewed
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