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ABSTRACT
Hyperplastic airway epithelial cells may be the cause for increased risk for lung cancer in patients with chronic lung diseases. The B-cell lymphoma 2 (Bcl-2) family member, Bcl-2-interacting killer (BIK), triggers cell death specifically in these hyperplastic cells because of adequate presence of Death-associated Protein Kinase 1 (DAPk1), BCL-2 Antagonist Killer (BAK), and Extracellular Signal-regulated Kinase 1/2 (ERK1/2). Therefore, BIK may be a useful tool to control the development of lung cancer in patients with chronic diseases.
Disclosure of potential conflicts of interest
No potential conflicts of interest were disclosed.
Additional information
Funding
National Institutes of Health (NIH) [grant number RO!HL068111].