| Budget Amount *help |
¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2013: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2012: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2011: ¥2,860,000 (Direct Cost: ¥2,200,000、Indirect Cost: ¥660,000)
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| Research Abstract |
EREG is overexpressed in non-small-cell lung cancers (NSCLCs) harboring KRAS, BRAF or EGFR mutations compared with small-cell lung cancers (SCLCs) or NSCLCs with wild-type KRAS/BRAF/EGFR. EREG expression was reduced by knockdown of mutant KRAS, BRAF or EGFR or by MEK or ERK inhibition in NSCLC cells. EREG expression positively correlated with KRAS copy number in KRAS-mutant NSCLCs. EREG was predominantly expressed in NSCLC tumors with pleural involvement, lymphatic permeation or vascular invasion and in KRAS-mutant adenocarcinomas. EREG expression is an independent prognostic marker and EREG overexpression along with KRAS mutations correlated with an unfavorable prognosis for lung adenocarcinoma patients. In KRAS-mutant and EREG overexpressing NSCLCs, EREG attenuation suppressed tumor growth and induced apoptosis. These results suggest that oncogenic KRAS-induced EREG overexpression contributes to an aggressive phenotype and could be a therapeutic target in oncogenic KRAS-driven NSCLC.
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