Dr. Pankaj Baral

Division of Biology
Departmental website

Our research focuses on identifying the role of the nervous system in chronic lung inflammation and development of lung adenocarcinoma. Lung adenocarcinoma is a sub-type of non-small cell lung cancer. Chronic inflammation, air pollution and other environmental causes are factors for developing lung cancers including lung adenocarcinoma.

Our lungs are innervated by sensory and autonomic (sympathetic and parasympathetic) nerve fibers that constantly interact with immune and epithelial cells in the lungs. Such interactions are crucial for tissue homeostasis, respiratory function and preventing threats. The nerve terminals in the lung release neuronal mediators (e.g., neuropeptides, neurotransmitters, lipid mediators) during homeostasis and upon detecting threats, and modulate the local immune landscape and tissue healing through binding with their cognate receptors expressed by immune and epithelial cells.

Neuronal activation or ablation has an impact on progression of melanoma and prostrate cancer in mice. However, it is largely unknown which neuronal population and mediator(s) are involved in lung cancer development and whether we can target the neuro-immune or neuro-epithelial communication pathways to treat lung cancer. We are investigating this using a genetically-engineered mouse model with Kras mutation and deletion of tumor suppressor p53.