| Project/Area Number |
17K16613
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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 |
Respiratory surgery
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| Research Institution | Fukushima Medical University |
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Principal Investigator |
Yamaura Takumi 福島県立医科大学, 医学部, 博士研究員 (20747240)
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| Project Period (FY) |
2017-04-01 – 2020-03-31
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| Project Status |
Completed (Fiscal Year 2019)
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| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2019: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000)
Fiscal Year 2018: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2017: ¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
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| Keywords | 肺癌 / KRAS / FAM83B / EGFR / 肺腺癌 / PD-L1 / バイオマーカー |
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| Outline of Final Research Achievements |
We focused on Family with sequence similarity 83, member B (FAM83B). In eight cases of KRAS mutant-lung adenocarcinoma (ADC), FAM83B was highly expressed in mucinous ADC tissue. Next, we compared FAM83B expression in lung ADC stratified by presence or absence of EGFR mutation, which is widely examined clinically and has an exclusive relation with KRAS mutation. FAM83B was significantly highly expressed in EGFR wild type group, that contain with a relatively high proportion of KRAS mutant-ADC. High FAM83B group had shorter postoperative recurrence-free survival and overall survival regardless of presence or absence of EGFR gene mutation significantly. Growth inhibition was confirmed by FAM83B RNAi in lung cancer-derived cell lines.
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| Academic Significance and Societal Importance of the Research Achievements |
本研究でFAM83Bが肺腺癌増殖と関連する因子であることが示された。肺腺癌の内KRAS遺伝子変異は粘液産生性肺腺癌との関連があり、この両者はそれぞれに治療抵抗性を示し予後不良な症例群であると報告されている。上記症例群でFAM83Bが高発現である、またFAM83Bを治療標的とした増殖阻害が臨床治療に応用できる可能性があると考えられ今後の検討を要する。肺癌診療への貢献が期待される。
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