Study on growth suppression of lung cancer by the inhibition of COX2,LOX, and EGFR for clinical application

点击翻译按钮获取中文摘要

This study showed that lipoxygenase inhibitors can inhibit proliferation of lung cancer cell lines in vitro in a dose-dependent manner, in part by inducing apoptosis. Moreover, we found that lipoxygenase inhibitors reduced the IC50 values of various anticancer agents, suggesting that the use of lipoxygenase inhibitors may be a promising therapeutic approach. Using a panel of 19 lung cancer cell lines, we observed the lack of association of gefitinib sensitivity with the expression of EGFR, HER2, HERS, and HER4. Our results also showed no apparent association between K-ras mutations and sensitivity to gefitinib. These data suggest that tumor EGFR expression is not clinically relevant for predicting response to gefitinib. In clinical studies, we found that about 40 % of Japanese patients with non-small cell lung cancer had EGFR mutations. The mutations were deletions or point mutations. EGFR mutations were significantly frequent in female, adenocarcinomas, and in never smokers, and EGFR mutations showed good -correlation with gefitinib effectiveness. These data suggest that EGFR mutations may help to define the patient population likely to benefit most from EGFR-targeted therapies.