Investigation of the molecular mechanisms that are involved in the survival of cancer cells in the presence molecular targeting drugs, and its implication for the development of novel drugs for cancer therapy.

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EGFR, EML4-ALK, and K-ras are major genetic mutations in non small cell lung cancers. Though inhibitors for EGFR and ALK are effective for each mutant cancers, K-ras inhibitor is not effective for cancers with mutated K-ras. It is not clear why the effects of inhibitor differ and how the tolerance is acquired. To clarify questions and to study new molecular targets, we examined gene expression profiles after addition of each inhibitor in NSCLC cell lines II-18, PC9, A549 that have mutated EGFR, EML4-ALK, and mutated K-ras, respectively. A microarray analysis of about 47000 genes of NSCLC cell lines, and we found 12 candidate genes that may be related to the drug resistance.