2012 Fiscal Year Final Research Report
Suppression of colon tumorigenesis by Ah receptor
| Project/Area Number |
22501001
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Carcinogenesis
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| Research Institution | Research Institute for Clinical Oncology, Saitama Cancer Center |
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Principal Investigator |
IKUTA Togo 埼玉県立がんセンター(臨床腫瘍研究所), 研究員 (00262072)
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| Co-Investigator(Renkei-kenkyūsha) |
KAWAJIRI Kaname 埼玉がんセンター, 臨床腫瘍研究所, 研究員 (50142112)
KOBAYASHI Yasuhito 埼玉県立循環器病センター (80425652)
KOIKE Manabu 放射線医学総合研究所, 研究員 (70280740)
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| Project Period (FY) |
2010 – 2012
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| Keywords | 炎症 / 大腸癌 / Ah レセプター |
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| Research Abstract |
Tumor suppressor function of Ah receptor(AhR) was shown by spontaneously developed cecal tumor in AhR-deficient mice. In order to investigate the role of AhR, we studied the production of inflammatory cytokines. Concentration of IL-1β and IL-6 produced in AhR-/- mice was significantly higher than AhR-/-・ASC-/- double mutated mice which showed reduced cecal carcinogenesis. We developed co-culture system constituted with colonic epithelial cells and macrophages and examined production of cytokines into the culture medium.
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[Journal Article] Association of germline or somatic TP53 missense mutation with oncogene amplification in tumors developed in patients with Li-Fraumeni or Li-Fraumeni-like syndrome.2011
Author(s)
Sugawara W, Arai Y, Kasai F, Fujiwara Y, Haruta M, Hosaka R, Nishida K, Kurosumi M, Kobayashi Y, Akagi K, Kaneko Y
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Journal Title
Genes Chromosomes Cancer
Volume: 50(7)
Pages: 535-545
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