Results describe the roles of MEK1/ERK and AKT/PKB pathways on the effects of granulocyte macrophage colony-stimulating factor (GM-CSF) and M-CSF on tumor progression of lung cancer.

analysis of the MEK1 mutation in lung adenocarcinoma

MEK1 mutations exclusive with EGFR, K-ras, and B-raf mutations at kinase domain is associated with lung cancer.

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

lung cancers with acquired resistance to EGFR inhibitors occasionally harbor BRAF gene mutations but lack mutations in KRAS, NRAS, or MEK1.

activation of RAF1-MEK1-ERK/AKT axis may determine the resistance of non-small cell lung cancer cell lines bearing wild type EGFR to erlotinib

MEK1 mutations define a distinct subset of lung cancers ( approximately 1%) with potential sensitivity to MEK inhibitors. mutations are predominantly transversions, in keeping with a strong association with smoking.

MEK1/2 inhibitor potentiated the anti-tumor effects of cisplatin in KRAS-dependent lung cancer cells and an animal model through inhibition of BIM degradation

MEK1/2 inhibitor trametinib showed similar PFS and a response rate as docetaxel in patients with previously treated KRAS-mutant-positive non-small cell lung carcinoma.

Data show that src kinases (SRC) and mitogen-activated protein kinase kinase 1 (MEK) co-inhibition by saracatinib and PD0325901 respectively can be broadly effective in tumor growth control of a wide panel of non-small cell lung cancer (NSCLC) cell lines.

MEK1 mutation is associated with central nervous system metastases of non-small cell lung cancer.

Decreased miR-16 expression may play a role in upregulating expression of MEK1 and promoting proliferation and invasion of lung cancer cells.