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Molecular and Physiologic Evidence for 5′CpG Island Methylation of the Endothelin B Receptor Gene in Lung Cancer*

Andrea J. Cohen, MD; Steven Belinsky, MD; Wilbur Franklin, MD; Scott Beard, MSc
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*From the Division of Pulmonary Science and Critical Care Medicine (Drs. Cohen and Franklin, and Mr. Beard), Denver Veterans Affairs Medical Center and University of Colorado Health Sciences Center; and Lovelace Research Institute (Dr. Belinsky), Albuquerque, NM.

Correspondence to: Andrea J. Cohen, MD, Assistant Professor of Medicine, Denver VA Medical Center, University of Colorado Health Sciences Center, 1055 Clermont Ave., Resp 111A, Denver, CO 80220



Chest. 2002;121(3_suppl):27S-28S. doi:10.1378/chest.121.3_suppl.27S-a
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We have previously reported molecular and physiologic evidence for an endothelin-1 autocrine loop in lung cancer. The endothelin-B receptor (ETBR), which is believed to counter-regulate endothelin-1, is not expressed in the majority of lung cancer cell lines.

We hypothesized that the inactivation of the ETBR is due to epigenetic silencing, specifically the hypermethylation of cytosine nucleotides of the 5CpG “island” surrounding the transcriptional start region of the ETBR gene. This process has been associated with the silencing of a number of tumor-suppressor genes.

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