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(Chest. 2004;125:79S.)
© 2004 American College of Chest Physicians

Lung Cancer Over 17 Years of Aspen Lung Conferences*

York E. Miller, MD and Robert L. Keith, MD, FCCP

* From the Division of Pulmonary Sciences and Critical Care Medicine (Drs. Miller and Keith), Denver Veterans Affairs Medical Center, Denver, CO; and the University of Colorado Comprehensive Cancer Center (Dr. Keith), University of Colorado Health Sciences Center, Boulder, CO.

Correspondence to: York E. Miller, MD, Pulmonary 111A, Denver Veterans Affairs Medical Center, 1055 Clermont St, Denver, CO 80220-3808; e-mail york.miller{at}uchsc.edu

This year’s Thomas L. Petty Aspen Lung Conference represents the second time that lung cancer has been the topic in the conference’s 45-year history. Seventeen years ago, Charles Scoggin chaired an Aspen Lung Conference on the Molecular and Cellular Biology of Lung Cancer. At that time, several oncogenes had been identified, but no tumor suppressor genes had yet been characterized. The Rb gene was first cloned later that year, and p53 was thought to be a tumor-associated antigen or an oncogene, not a tumor suppressor. No presenters discussed specific oncogenes in lung cancer, although there was a talk on alterations in DNA methylation. The conference focused on the general principles of cancer biology, but the specific mutations and alterations in gene expression that underlie the neoplastic process were largely unknown. Few of the participants were pulmonologists, and the research was not yet at the stage at which it could be readily translated to the clinical arena.

There have been many advances in our knowledge of lung carcinogenesis in the intervening 17 years. We have greatly improved our understanding of the mutations, epigenetic changes, alterations in gene and protein expression, and intracellular and intercellular signaling that occur as the respiratory epithelium changes from normal to cancerous. This year’s conference was focused on how we can apply this knowledge to the definition of individuals or groups who are at high risk for lung cancer, and how we can effect early intervention in the carcinogenesis process. The "State of the Art" speakers provided new syntheses of their topics, and many of the attendees participated in lively interchanges. David Carbone, the Conference Summarizer, gave an outstanding perspective on the science presented and a vision of the future.

David Carbone also touched on the importance of collaboration between the pulmonologists and other subspecialists, and the scientists who study or treat lung cancer patients. Traditionally, the Aspen Lung Conference has consisted largely of pulmonary scientists and clinicians. The pulmonary community now has many investigators (including Tom Petty, for whom the conference is named) who are interested primarily in the pathogenesis, prevention, detection, and treatment of preneoplasia or early lung cancer, but we are not yet engaged actively in the treatment of disseminated disease. Concepts that were first developed by researchers who were interested in cancer, such as the expansion of clones of cells with mutations or epigenetic alterations, have now been applied to other forms of lung disease, including interstitial fibrosis and pulmonary hypertension. We do not yet know the mechanistic details of the shared pathogenesis of COPD and lung cancer. There is much to be gained from the collaboration between scientists primarily interested in neoplastic tobacco-induced lung disease and those interested in nonneoplastic tobacco-induced lung disease.

Seventeen years ago, we heard presentations that promised a better understanding of the molecular pathogenesis of lung cancer, and we now have made major advances that are being applied to diagnosis and treatment in the clinic. This year, we heard presentations that promised a better definition of risk and effective new early interventions. We hope that it will not be another 17 years until lung cancer is again the topic of the Thomas L. Petty Aspen Lung Conference, and we are confident that the interim progress will be equally impressive.


    Acknowledgements
 
We thank the Francis Family Foundation for their continued support of the Parker B. Francis Lectureship. We also appreciate the generous support of all of the sponsors of this year’s conference.





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