Studies on digestive system cancer metastasis using mouse models
Project/Area Number |
25253022
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Research Category |
Grant-in-Aid for Scientific Research (A)
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Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Pathological medical chemistry
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Research Institution | Kyoto University |
Principal Investigator |
TAKETO Makoto 京都大学, 医学(系)研究科(研究院), 特命教授 (70281714)
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Co-Investigator(Kenkyū-buntansha) |
KAKIZAKI Fumihiko 京都大学, 大学院医学研究科, 特定研究員 (00609076)
SONOSHITA Masahiro 京都大学, 大学院医学研究科, 准教授 (80511857)
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Project Period (FY) |
2013-04-01 – 2016-03-31
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Project Status |
Completed (Fiscal Year 2015)
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Budget Amount *help |
¥46,280,000 (Direct Cost: ¥35,600,000、Indirect Cost: ¥10,680,000)
Fiscal Year 2015: ¥14,300,000 (Direct Cost: ¥11,000,000、Indirect Cost: ¥3,300,000)
Fiscal Year 2014: ¥14,300,000 (Direct Cost: ¥11,000,000、Indirect Cost: ¥3,300,000)
Fiscal Year 2013: ¥17,680,000 (Direct Cost: ¥13,600,000、Indirect Cost: ¥4,080,000)
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Keywords | 消化器がん / 浸潤 / 転移 / 予後マーカー / AES / NOTCH / ABL / TRIO / がん / 消化器 / ケモカイン / Notchシグナル / TGF-betaシグナル / 予後診断 / がん転移 |
Outline of Final Research Achievements |
(1)In the invasion and metastasis model where mouse colon cancer cells are disseminated to the liver from spleen, we found two phase reaction of the host bone marrow-derived cells. In the early phase, neutrophils are recruited and in the late phase, fibrocytes. MMP9 and MMP2 are produced by these types of cells, respectively, which is critical for cancer invasion and metastasis. (2)One of the genes induced by Notch signaling transcription in colon cancer cells is DAB1 of which product is tyrosine-phosphrylated by ABL kinase, which receiprocally activates ABL autophosphorylation. As a result, TRIO Y2681 is phosphorylated, which shows a strong correlation with poor prognosis as a novel diagnostic marker.
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Report
(5 results)
Research Products
(28 results)
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[Journal Article] Loss of SMAD4 Promotes Colorectal Cancer Progression by Accumulation of Myeloid-Derived Suppressor Cells through the CCL15-CCR1 Chemokine Axis2016
Author(s)
Susumu Inamoto1, Yoshiro Itatani1,2, Takamasa Yamamoto1, Sachiko Minamiguchi3, Hideyo Hirai4, Masayoshi Iwamoto1, Suguru Hasegawa1, Makoto Mark Taketo1,2, Yoshiharu Sakai1, and Kenji Kawada1,*
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Journal Title
Clin. Cancer Res.
Volume: 22
Issue: 2
Pages: 492-501
DOI
Related Report
Peer Reviewed / Int'l Joint Research / Acknowledgement Compliant
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[Journal Article] Suppressing TGFβ signaling in regenerating epithelia in an inflammatory microenvironment is sufficient to cause invasive intestinal cancer.2015
Author(s)
Oshima H, Nakayama M, Han TS, Naoi K, Ju X, Maeda Y, Robine S, Tsuchiya K, Sato T, Sato H, Taketo MM, Oshima M.
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Journal Title
Cancer Res.
Volume: 75
Pages: 766-776
Related Report
Peer Reviewed / Int'l Joint Research
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[Journal Article] Loss of SMAD4 from colorectal cancer cells promotes CCL15 expression to recruit CCR1+ myeloid cells and facilitate liver metastasis.2013
Author(s)
Itatani Y, Kawada K, Fujishita T, Kakizaki F, Hirai H, Matsumoto T, Iwamoto M, Inamoto S, Hatano E, Hasegawa S, Maekawa T, Uemoto S, Sakai Y, Taketo MM
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Journal Title
Gastroenterol
Volume: 145(5)
Issue: 5
Pages: 1064-1075
DOI
NAID
Related Report
Peer Reviewed
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[Presentation] Loss of Smad4 in Colorectal Cancer Cells Promotes CCL15 Expression to Recruit CCR1+ Myeloid Cells and Facilitate Liver Metastasis.2013
Author(s)
Yoshiro Itatani,Kawada K, Fujishita T, Kakizaki F, Hirai H, Matsumoto T, Iwamoto M, Inamoto S, Hatano E, Hasegawa S, Maekawa T, Uemoto S, Sakai Y, Taketo MM
Organizer
American College of Surgeons
Place of Presentation
Washington, DC, USA
Related Report
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