<?xml version='1.0' encoding='UTF-8'?><xml><records><record><source-app name="HighWire" version="7.x">Drupal-HighWire</source-app><ref-type name="Journal Article">17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">SUENAGA, MITSUHIRO</style></author><author><style face="normal" font="default" size="100%">YAMAMOTO, MASATATSU</style></author><author><style face="normal" font="default" size="100%">TABATA, SHO</style></author><author><style face="normal" font="default" size="100%">ITAKURA, SUSUMU</style></author><author><style face="normal" font="default" size="100%">MIYATA, MASAAKI</style></author><author><style face="normal" font="default" size="100%">HAMASAKI, SHUICHI</style></author><author><style face="normal" font="default" size="100%">FURUKAWA, TATSUHIKO</style></author></authors><secondary-authors></secondary-authors></contributors><titles><title><style face="normal" font="default" size="100%">Influence of Gefitinib and Erlotinib on Apoptosis and c-MYC Expression in H23 Lung Cancer Cells</style></title><secondary-title><style face="normal" font="default" size="100%">Anticancer Research</style></secondary-title></titles><dates><year><style  face="normal" font="default" size="100%">2013</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2013-04-01 00:00:00</style></date></pub-dates></dates><pages><style  face="normal" font="default" size="100%">1547-1554</style></pages><volume><style face="normal" font="default" size="100%">33</style></volume><issue><style face="normal" font="default" size="100%">4</style></issue><abstract><style  face="normal" font="default" size="100%">Background: Gefitinib and erlotinib are inhibitors of epidermal growth factor receptor tyrosine kinase. The effects of these tyrosine kinase inhibitors on RAS-mutated cancer cells are unclear. Materials and Methods: Influence of gefitinib and erlotinib treatment was examined in H23 adenocarcinoma and A431 epidermoid carcinoma cells. The WST-1 assay was performed for evaluating cell growth. The phosphorylation status of extracellular-signal-regulated kinases (ERK) and AKT (protein kinase B) was examined by western blot. Flow cytometry was used for analyzing cell-cycle status and apoptosis detection. Results: In H23 cells, 20 μM erlotinib suppressed growth, while gefitinib did not suppress proliferation after 48 h of treatment. Neither gefitinib nor erlotinib affected the phosphorylation of ERK and AKT in H23 cells. Erlotinib augmented the sub-G1 population of H23 cells, while gefitinib reduced it. Conclusion: In H23 cells, erlotinib accelerated apoptosis, while gefitinib induced G1 arrest.</style></abstract></record></records></xml>