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Metastatic Cancer While Receiving Continuous Prostacyclin Therapy*

Karen A. Fagan, MD; Todd M. Bull, MD; David B. Badesch, MD, FCCP; Norbert F. Voelkel, MD
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*From the Department of Medicine, Division of Pulmonary Sciences and Critical Care Medicine, Pulmonary Hypertension Center, University of Colorado Health Sciences Center, Denver, CO.

Correspondence to: Karen Fagan, MD, 4200 East Ninth Ave, C-272, Denver, CO 80262; e-mail: karen.fagan@uchsc.edu



Chest. 2005;128(6_suppl):619S-620S. doi:10.1378/chest.128.6_suppl.619S-a
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Prostacyclin and its derivatives are reported to decrease tumor metastases in several animal models. Potential mechanisms include the modulation of endothelial cell adhesion molecule expression, decreased adhesion of tumor cells to the subendothelial matrix, decreased tumor cell-platelet aggregation, decreased tumor cell-induced endothelial cell retraction, and decreased growth of micrometastases. The inhibition of cyclooxygenase-2 has been demonstrated to decrease the formation of colon adenomas and the development of colon carcinoma. Cancer chemoprevention trials using prostacyclin are underway. Thus, we hypothesized that patients receiving prostacyclin treatment are relatively protected from the development of metastatic malignancy.

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