Common molecular mechanisms regulating murine breast cancer stem cells and leukemia stem cells
| Project/Area Number |
26670135
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
General medical chemistry
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| Research Institution | Hiroshima University (2015)
Kanazawa University (2014) |
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Principal Investigator |
NAKA Kazuhito 広島大学, 原爆放射線医科学研究所, 准教授 (70372688)
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| Project Period (FY) |
2014-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2015: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2014: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
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| Keywords | がん幹細胞 / 乳がん幹細胞 / CML幹細胞 / 代謝産物 / メタボローム / 乳がん / 休眠状態 / MMTV-PyVT / 再発 |
|---|
| Outline of Final Research Achievements |
Although it is now widely accepted that cancer stem cells are the cell-of-origin of the vast majority of mature cancer cells and are reportedly responsible for the recurrence of disease following anti-cancer therapy, the molecular mechanisms regulating cancer stem cells in epithelial tumors has remained elusive. The biological characteristics of mature cancer cells appear to be distinct among breast cancer cells originate from endoderm and leukemia cells originate from mesoderm. However, I hypothesized that common molecular mechanisms such as stem cell quiescence and/or therapeutic resistance might sustain the long-term survival of breast cancer stem cells and chronic myelogenous leukemia (CML) stem cells. In this study, I used sophisticated metabolomics techniques to investigate the distinct and common molecular mechanisms maintaining self-renewal capacity of murine breast cancer stem cells and murine CML stem cells in vivo.
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Report
(3 results)
Research Products
(20 results)
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[Journal Article] Novel oral transforming growth factor-β signaling inhibitor EW-7197 eradicates CML-initiating cells.2016
Author(s)
Naka K, Ishihara K, Jomen Y, Jin CH, Kim DH, Gu YK, Jeong ES, Li S, Krause DS, Kim DW, Bae E, Takihara Y, Hirao A, Oshima H, Oshima M, Ooshima A, Sheen YY, Kim SJ, Kim DK.
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Journal Title
Cancer Sci.
Volume: 107
Issue: 2
Pages: 140-148
DOI
Related Report
Peer Reviewed / Open Access / Int'l Joint Research / Acknowledgement Compliant
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[Journal Article] Dipeptide species regulate nutrient signalling essential for the maintenance of chronic myelogenous leukaemia stem cells.2015
Author(s)
Naka K, Jomen Y, Ishihara K, Kim J, Ishimoto T, Bae E, Mohney R, Stirdivant SM, Oshima H, Oshima M, Kim DW, Nakauchi H, Takihara Y, Kato Y, Ooshima A, Kim SJ.
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Journal Title
Nature Communication
Volume: 6
Issue: 1
Pages: 8039-8039
DOI
Related Report
Peer Reviewed / Open Access / Int'l Joint Research
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[Journal Article] Homozygous Deletions at 3p22, 5p14, 6q15, and 9p21 Result in Aberrant Expression of Tumor Suppressor Genes in Gastric Cancer.2015
Author(s)
Lee B., Yoon K.Y., Lee S.H., Kang J.M., Kim J.I., Shim S.H., Kim H.-M., Song S.H., Naka K., Kim A.K., Yang H.-K., Kim S.J.
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Journal Title
Genes, Chromosomes and Cancer.
Volume: 54
Issue: 3
Pages: 142-155
DOI
Related Report
Peer Reviewed / Int'l Joint Research
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[Book] 血液内科2015
Author(s)
仲 一仁
Total Pages
6
Publisher
CML幹細胞を標的とする治療戦略の可能性
Related Report
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