Abstract
Progression and metastasis of cancer proceeds in the context of a host response that includes interactions with immune cells that can both attenuate and paradoxically promote the process of metastasis. Growing evidence demonstrating the role of the inflammatory response in carcinogenesis is shedding light on a functional relationship between the host immune system and the malignant neoplasm. The interaction between neoplasm and the immune system can be described with the concepts of (1) cancer immunosurveillance, (2) cancer immunoediting, (3) complicity of the host cellular networks in lung tumorigenesis, and (4) tumor-mediated immunosuppression. Understanding the molecular mechanisms involved in inflammation and lung carcinogenesis provides insight for new drug development that target reversible, non-mutational events in the chemoprevention and treatment of lung cancer.
Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
