| Project/Area Number |
15K10148
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Digestive surgery
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| Research Institution | Kitasato University |
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Principal Investigator |
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| Research Collaborator |
YAMASHITA Keishi 北里大学, 医学部, 教授
WATANABE Masahiko 北里大学, 医学部, 教授
SATO Takeo 北里大学, 医学部, 講師
NAKAMURA Takatoshi 北里大学, 医学部, 准教授
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2017: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2016: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2015: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Keywords | 術前放射線化学療法 / 放射線感受性 / 進行直腸癌 / CD163 / 腫瘍関連マクロファージ / 直腸癌 / CRBP1 / 骨髄由来細胞 |
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| Outline of Final Research Achievements |
We aimed to predict sensitivity to neoadjuvant chemoradiotherapy in advanced rectal cancer. Analysis of routine peripheral leukocyte fraction revealed that patients with high monocyte fraction showed poor prognosis. Immunohistochemistry indicate that accumulation of CD163+ tumor-associated macrophage was associated with refractoriness to neoadjuvant chemoradiotherapy among immunocytes (eg. myeloid-derived suppressor cells, macrophages) derived from circulating monocytes. Comprehensive molecular exploration identified CRBP1 gene as a determinant of radiation sensitivity. CRBP1 silencing by its promoter methylation was related to refractoriness to neoadjuvant chemoradiotherapy in patients with advanced rectal cancer.
In the next steps, we analyze the network between CRBP1 and recruitment of CD163 macrophage including cytokine system. These results would lead to a novel approach to clarify a mechanism of chemoradiosensitivity.
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