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Lung Cancer Prevention^*

The Guidelines

^* From the Norris Cotton Cancer Center and Dartmouth Medical School (Drs. Dragnev and Dmitrovsky), Lebanon, NH; and the Pulmonary Section (Dr. Stover), Department of Medicine, Memorial Sloan-Kettering Cancer Center, New York, NY.

Correspondence to: Konstantin H. Dragnev, MD, Hematology/Oncology Section, Department of Medicine, Dartmouth-Hitchcock Medical Center, Lebanon, NH 03756; e-mail: dragnev{at}dartmouth.edu

Lung carcinogenesis is a chronic and multi-step process resulting in malignant lung tumors. This progression from normal to neoplastic pulmonary cells or tissues could be arrested or reversed through pharmacologic treatments, which are known as cancer chemoprevention. These therapeutic interventions should reduce or avoid the clinical consequences of lung cancer by treating early neoplastic lesions before the development of clinically evident signs or symptoms of malignancy. Preclinical, clinical, and epidemiologic findings relating to different classes of candidate chemopreventive agents provide strong support for lung cancer prevention as an attractive therapeutic strategy. Smoking prevention and smoking cessation represent an essential approach to reduce the societal impact of tobacco carcinogenesis. However, even if all the goals of the national antismoking efforts were met, there still would be a large population of former smokers who would be at increased risk for lung cancers. Lung cancer also can occur in those persons who never have smoked. This article focuses on what is now known about pharmacologic strategies for lung cancer prevention. Randomized clinical trials using ß-carotene, retinol, isotretinoin or N-acetyl-cysteine did not show benefit for primary and tertiary lung cancer prevention. There is also evidence that the use of ß-carotene and isotretinoin for lung cancer chemoprevention in high-risk individuals may increase the risk for lung cancer, especially in individuals who continue to smoke. There is a need for relevant in vitro models to identify pathways that activate chemopreventive effects in the lung. An improved understanding of cancer prevention mechanisms should aid in the design of clinical trials and in the validation of candidate chemopreventive targets as well as the discovery of new targets. Until such studies are completed, no agent or combination of agents should be used for lung cancer prevention outside of a clinical trial.

Key Words: chemoprevention • epidermal growth factor receptor • G1 cyclin • lung cancer • retinoids

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