individualization of anti-kinase drugs for Asian cancers using genomic and proteomic analysis

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Whereas cancers with amplified MET gene, an oncogene, are potentially good target of MET kinase inhibitors, emergence of acquired resistance is highly expected. Our current study using MET-amplified gastric cancer cell lines suggested that both increase in copy number and Y1230H mutation of MET gene could cause acquired resistance. While MET copy number decreased in the absence of MET inhibitor and cells regained sensitivity to it, Y1230H mutation was irreversible alteration. This finding suggested possibility of individualized treatment based on acquired resistance mechanism in the future. Our another study using HER2-amplified gastric cancer cell lines showed that suppression of phosphorylated S6K is important molecular event to enhance 5FU-induced apoptosis, so that 5FU/everolimus combination was suggested to be attractive treatment strategy for gastric cancer with HER2 amplification.