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Prostacyclin in Human Non-small Cell Lung Cancers*

Patrick Nana-Sinkam, MD; Heiko Golpon, MD; Robert L. Keith, MD; Ryan J. Oyer, MS; Sylk Sotto-Santiago, MBA; Mark D. Moore, BS; Wilbur Franklin, MD; Raphael A. Nemenoff, PhD; Mark W. Geraci, MD
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*From the Division of Pulmonary Sciences and Critical Care Medicine (Drs. Nana-Sinkam, Golpon, Keith, and Geraci, and Messrs. Oyer, Sotto-Santiago, and Moore), Division of Nephrology (Dr. Nemenoff), and Department of Pathology (Dr. Franklin), University of Colorado Health Sciences Center, Denver, CO.

Correspondence to: Patrick Nana-Sinkam, MD, Division of Pulmonary Sciences and Critical Care Medicine, University of Colorado Health Sciences Center, 4200 East 9th Ave, Box C272, Denver, CO 80262; e-mail: patrick.nana-sinkam@uchsc.edu



Chest. 2004;125(5_suppl):141S. doi:10.1378/chest.125.5_suppl.141S
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Lung cancer is the leading cause of cancer death in men and women in the United States. The cyclooxygenase pathway has a role in colon cancer chemoprevention and a potential role in lung cancer. Cyclooxygenase inhibition reduces lung cancer multiplicity in a murine model. We have shown that prostacyclin synthase (PGI2S) overexpression protects against tumor development in a transgenic mouse model. We hypothesize that eicosanoid balance is of importance in lung tumorigenesis, and propose a model for transcriptional regulation of PGI2S.

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