BIM is induced by lung cancer cell lines that are sensitive to erlotinib but not by those resistant.

Apoptosis induction by MEK1/2 inhibition in human lung cancer cells is mediated by Bim.

Data show that ALK inhibitor-induced apoptosis is mediated both by BIM upregulation resulting from inhibition of ERK signaling as well as by survivin downregulation resulting from inhibition of STAT3 signaling in EML4-ALK-positive lung cancer cells.

Bim is required for the combretastatin-A4 induced cell death in the H460 lung cancer cell line via activation of the mitochondrial signalling pathway.

BIM RNA levels in EGFR-mutant lung cancer specimens predicted response and duration of clinical benefit from EGFR inhibitors.

Investigated the function of Bim during DHA-induced apoptosis in human lung adenocarcinoma cell lines.Confocal imaging showed the translocation of Bim to endoplasmic reticulum (ER) rather than mitochondria during DHA-induced apoptosis.

Loss of BIM expression is associated with drug resistance in non-small cell lung cancer.

Bcl-2 overexpression induced up-regulation of the proapoptotic protein Bim in lung cancer cells.

BIM deletion polymorphism is associated with non-small-cell lung cancer with epidermal growth factor receptor mutation.

MiR-192 binded to Bim 3'-UTR and negatively regulated Bim expression at the post-transcriptional level in lung adenocarcinoma cells.

The BIM deletion polymorphism was not associated with lung cancer susceptibility. Furthermore, the BIM polymorphism is not associated with EGFR mutant lung cancer.

mRNA expression of BIM and MTOR in 57 patients with EGFR-mutant non-small-cell lung cancer.

BIM deletion polymorphism does not account for intrinsic resistance to EGFR-TKI in Patients With lung Adenocarcinoma

this study shows that BIM deletion polymorphisms are associated with a poor clinical response to erlotinib and represents an independent prognostic factor for patients with EGFR positive non-small-cell lung cancer

These findings indicate the importance of developing HDAC3-selective inhibitors, and their combined use with osimertinib, for treating EGFR-mutated lung cancers carrying the BIM deletion polymorphism

Modulation of MEK/ERK-dependent Bim and Mcl-1 degradation critically mediates sensitivity and resistance of EGFR-mutant non-small cell lung cancer (NSCLC)cells to AZD9291 and hence is an effective strategy to overcome acquired resistance to AZD9291

The BIM deletion polymorphism was an independent indicator of shorter survival in patients with advanced lung adenocarcinoma

BIM deletion polymorphism was associated with significantly shorter progression-free survival (PFS) and slightly shorter overall survival (OS), compared to the WT group. Moreover, patients with BIM deletion polymorphism showed significantly inferior response to EGFR TKIs. In conclusion, our analysis confirmed that lung cancer patients harboring the BIM deletion have inferior survival and TKI responses.

Negative expression of HuR and Bim correlates with lower EGFR-tyrosine kinase inhibitors sensitivity in tumor tissues obtained from EGFR-mutant nonsmall cell lung cancer patients.

Clinical significance of BIM deletion polymorphism in chemoradiotherapy for non-small cell lung cancer.