This relationship between EMT and loss of BIM is not restricted to <i>EGFR</i>-mutant lung cancers, as it was also observed in <i>KRAS</i>-mutant lung cancers and large datasets, including different cancer subtypes.<b>Conclusions:</b> Altogether, these data reveal a novel mechanistic link between EMT and resistance to lung cancer targeted therapies.<i></i>.
A review of the literature revealed 60 mutation hotspots in seven target genes (EGFR, KRAS, PIK3CA, BRAF, ERBB2, NRAS, and BIM) that are closely related to EGFR TKI resistance to lung cancer.
A systematic review and meta-analysis of individual patient data on the impact of the BIM deletion polymorphism on treatment outcomes in epidermal growth factor receptor mutant lung cancer.
Depletion of BIM and overexpression of survivin each inhibited TAE684-induced apoptosis, suggesting that both upregulation of BIM and downregulation of survivin contribute to TAE684-induced apoptosis in EML4-ALK-positive lung cancer cells.
We found that AZD6244 elicited a large increase of Bim proteins and a smaller increase of PUMA and NOXA proteins, and induced cell death in sensitive lung cancer cell lines, but had no effect on other Bcl-2 related proteins in those cell lines.