Abstract
Background: The approval and use of epidermal growth factor receptor-tyrosine kinase inhibitors (EGFR-TKIs) in EGFR-mutant NSCLC has been a breakthrough in clinic. The activation of compensatory pathways of PI3 K/ AKT and/or MEK/MAPK modulates cell survival and drug resistance of lung adenocarcinoma (LUAC). As a convergent downstream signaling node and the determinant, BAD is a potential target to inhibit cell survival and to overcome EGFR TKI resistance in LUAC treatment.
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