Keratin 17 controls cancer characteristics in oral mucosa: Analysis of the mechanisms of oncogenesis through the mTOR signaling
Project/Area Number |
26861706
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Research Category |
Grant-in-Aid for Young Scientists (B)
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Allocation Type | Multi-year Fund |
Research Field |
Surgical dentistry
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Research Institution | Niigata University |
Principal Investigator |
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Project Period (FY) |
2014-04-01 – 2017-03-31
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Project Status |
Completed (Fiscal Year 2016)
|
Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2016: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2015: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2014: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
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Keywords | 口腔扁平上皮癌 / 上皮内癌 / keratin 17 / 14-3-3 sigma / mTOR / Keratin17 |
Outline of Final Research Achievements |
We determined immunohistochemical profiles of 14-3-3 sigma, Keratin(K) 17 and mTOR pathway markers in tissue specimens of oral borderline malignancies and SCC. We selected from the surgical pathology files of Niigata University Hospital surgical specimens of oral mucosa, which had been removed due to SCC or CIS, and simultaneously contained in addition to areas of SCC/CIS areas of epithelial dysplasia and/or normal epithelium. All the specimens were routinely fixed in 10% formalin and embedded in paraffin. Serial 3-lm sections were cut from paraffin blocks. One set of the sections was stained with hematoxylin and eosin (HE) and was used for reevaluation of histological diagnosis, and the other sets were used for immunohistochemistry (K17, 14-3-3 sigma, Akt, phospho-Akt, S6K1, phospho-S6K1, 4E-BP1, phospho-4E-BP1). As a result, although 14-3-3 sigma and K17 were co-expressed in oral SCC and CIS tissues, activation of the mTOR signaling pathway was not recognized immunohistologically.
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Report
(4 results)
Research Products
(1 results)