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━━ Apoptosis resistance has recently been reported to be a factor which induces resistance to EGFR-TKI at an early stage in EGFR mutant lung cancer. BIM is a BH3-only pro-apoptotic protein, and its upregulation is required for apoptotic induction by EGFR-TKI. Notably, a BIM deletion polymorphism occurs naturally in 13% of East Asian individuals, impairing the generation of the pro-apoptotic isoform required for EGFR-TKI, therefore conferring an inherent drug-resistant phenotype. We previously reported that an HDAC inhibitor, vorinostat, could increase the expression of functional BIM protein, which was sufficient to restore gefitinib sensitivity. An investigator-initiated Phase I trial using vorinostat and gefitinib combination therapy in a multi-institution study for EGFR mutant lung cancer patients who have a BIM polymorphism is currently under way. (JJLC. 2015;55:941-947)

Development of Therapy for Overcoming EGFR-TKI Resistance due to <i>BIM</i> Polymorphisms