2017 Fiscal Year Final Research Report
Carcinogenesis and progression of high grade EGFR-mutated lung adenocarcinoma
Project/Area Number |
15K08365
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Human pathology
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Research Institution | Yokohama City University |
Principal Investigator |
OHASHI Kenichi 横浜市立大学, 医学研究科, 教授 (40231203)
|
Co-Investigator(Kenkyū-buntansha) |
奥寺 康司 横浜市立大学, 医学部, 准教授 (10326027)
立石 陽子 横浜市立大学, 医学部, 助教 (20644438)
梅田 茂明 横浜市立大学, 医学部, 助教 (30644439)
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Project Period (FY) |
2015-04-01 – 2018-03-31
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Keywords | 肺がん / 腺がん / 病理学 / EGFR / 間質性肺炎 / 粘液 |
Outline of Final Research Achievements |
Surgically resected lung adenocarcinomas with and without lymph node metastasis and biopsy samples from inoperably advanced tumors were examined pathologically. The micropapillary element was clarified to be an exclusive determinant of malignant potential in EGFR-mutated lung adenocarcinomas. Pathological features and mucin family protein expression profile of idiopathic interstitial pneumonia (IIP)-associated pulmonary adenocarcinomas was investigated. In the IIP group, expression of MUC1, MUC7 and MUC21 was lower, and that of MUC4, MUC5AC, MUC5 and MUC9 was higher than non-IIP group. In the TRU group cases, IIP group cases showed distinctly lower expression of MUC1, and higher expression of MUC4, MUC5B and MUC9 than non-IIP group cases. Expression of MUC21 was tightly linked to micropapillary and low papillary lepidic variants.IIP-associated pulmonary adenocarcinomas, especially those of TRU group, showed specific expression profile of mucin family proteins.
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Free Research Field |
人体病理学
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