| Project/Area Number |
16K19072
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Human pathology
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| Research Institution | Tokyo Medical University |
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Principal Investigator |
Hirai Hideaki 東京医科大学, 医学部, 助教 (00770744)
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| Project Period (FY) |
2016-04-01 – 2019-03-31
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| Project Status |
Completed (Fiscal Year 2018)
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| Budget Amount *help |
¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
Fiscal Year 2018: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2017: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2016: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
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| Keywords | 胃癌 / 食道癌 / 唾液腺導管癌 / 癌微小環境 / 時計遺伝子 / DEC / AR / HER2 |
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| Outline of Final Research Achievements |
By focusing on the amount of stromal component, we subclassified the poorly differentiated gastric adenocarcinoma of solid type into the two groups: medullary carcinoma and non-medullary carcinoma. The medullary carcinomas less frequently displayed lymphatic invasion, venous invasion, and lymph node metastasis, compared with the non-medullary carcinoma. The patients with medullary carcinomas significantly showed better disease-free survival.
Furthermore, alterations in expression of apoptosis-related markers in human esophageal squamous cell carcinoma TE-11 cells treated with cisplatin were examined by western blot, while overall cell viability and apoptosis were analyzed by MTS assay and hematoxylin and eosin staining, respectively. We showed DEC2 exhibits anti-apoptotic effects in TE-11 esophageal squamous cell carcinoma cells.
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| Academic Significance and Societal Importance of the Research Achievements |
本研究では、胃や食道などの消化器癌における癌微小環境や、時計遺伝子発現の役割の一部を明らかにした。消化器癌ではDEC2を抑制することでアポトーシスが促進されるため、DEC2が治療標的になりうることが示唆された。これらの研究成果は、消化器癌の新たな治療戦略の構築に寄与するものと考えられる。
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