| Budget Amount *help |
¥16,250,000 (Direct Cost: ¥12,500,000、Indirect Cost: ¥3,750,000)
Fiscal Year 2016: ¥5,850,000 (Direct Cost: ¥4,500,000、Indirect Cost: ¥1,350,000)
Fiscal Year 2015: ¥5,850,000 (Direct Cost: ¥4,500,000、Indirect Cost: ¥1,350,000)
Fiscal Year 2014: ¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
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| Outline of Final Research Achievements |
As immune-mediated factors which are critical to reduce sensitibity and/or trigger resistance to EGF-TKI agains NSCLC through the analysis of novel spontaneous NSCLC models and clinical samples, we identified signaling pathways related to differentiation and activation of M2 macrophages and MDSC, two major immunosuppressive myeloid cells, as important factor to predict low sensitivity and emergence of resistant-associated mutation (T790M) to EGF-TKI against lung adenocarcinoma. Moreover, the combination of CSF1 inhibitors and EGF^TKI dramatically reduced incidence of spontaneous lung adenocarcinoma in mouse models. On the other hands, there are no involvement of immune checkpoint pathways as immune factors to regulate lung adenocarcinoma.It is important to clarify novel immune-mediated mechanisms other than immune checkpoint such as PD-1 to regulate responsiveness of EGFR-TKI against lung adenocarcinomas.
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