| Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2011: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2010: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2009: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Research Abstract |
Tyrosine kinase inhibitor(TKI) is effective for lung cancers with EGFR mutation, but these tumors eventually acquire drug resistance. In the present study, we found that some TKI-treated tumors mainly composed of EGFR-wild tumor dells while the EGFR-mutant ones vanished or markedly decreased, and their pre-treated tumors contained EGFR-wild tumor cells. Furthermore, with surgically resected TKI-untreated cases, we showed that most EGFR-mutant tumors also contained EGFR-wild tumor cells. Thus, multiple mechanisms underline acquired TKI resistance, and besides the reported secondary EGFR T790M mutation and adaptive Met amplification, the selective survival of the preexisting TKI-resistant EGFR-wild tumor cells also contributes to the drug acquisition.
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