{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,8,2]],"date-time":"2025-08-02T16:34:59Z","timestamp":1754152499557,"version":"3.41.2"},"reference-count":45,"publisher":"Wiley","issue":"12","license":[{"start":{"date-parts":[[2025,6,18]],"date-time":"2025-06-18T00:00:00Z","timestamp":1750204800000},"content-version":"vor","delay-in-days":17,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Thoracic Cancer"],"published-print":{"date-parts":[[2025,6]]},"abstract":"<jats:title>ABSTRACT<\/jats:title><jats:p>Lung cancer is the most common and deadly type of cancer. Our previous study showed that carvedilol, a \u03b2\u2010blocker, can prevent lung cancer induced by benzo(a)pyrene [B(a)P]. Carvedilol is a 1:1 racemic mixture of S\u2010 and R\u2010carvedilol, with S\u2010carvedilol acting as a \u03b2\u2010adrenergic blocker, while R\u2010carvedilol lacks \u03b2\u2010blocking activity. Despite this, a previous study showed that R\u2010carvedilol effectively prevents UV\u2010induced skin cancer. This study aimed to determine whether carvedilol's lung cancer prevention relies on its \u03b2\u2010blocking activity. We compared the effectiveness of S\u2010 and R\u2010carvedilol in preventing lung cancer induced by B(a)P and its metabolite, benzo(a)pyrene diol epoxide (BPDE), both in\u00a0vivo and in\u00a0vitro. Our results showed that S\u2010 and R\u2010carvedilol equally prevent malignant transformation of the human bronchial epithelial cell line (BEAS\u20102B) induced by BPDE. Furthermore, both S\u2010 and R\u2010carvedilol significantly inhibit the B(a)P\u2010induced activation of the aryl hydrocarbon receptor (AhR)\/xenobiotic responsive element (XRE) and mRNA expression of CYP1A1 in BEAS\u20102B cells. In mice, daily administering S\u2010 or R\u2010carvedilol for 7\u2009days before exposing them to B(a)P resulted in a significant decrease in the levels of lactate dehydrogenase and malondialdehyde and prevented inflammatory cell infiltration and histopathologic abnormalities in mouse lungs. Exposure to B(a)P caused the development of lung tumors, but treating the mice with S\u2010 or R\u2010carvedilol for 23\u2009weeks significantly reduced the number and size of these tumors. The results were confirmed by H&amp;E\u2010stained images of the mouse lungs. These findings support the hypothesis that carvedilol prevents B(a)P\u2010induced lung inflammation and carcinogenesis independently of \u03b2\u2010blockade.<\/jats:p>","DOI":"10.1111\/1759-7714.70109","type":"journal-article","created":{"date-parts":[[2025,6,19]],"date-time":"2025-06-19T02:20:46Z","timestamp":1750299646000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["S\u2010 and R\u2010Carvedilol Prevent Benzo(a)pyrene\u2010Induced Lung Carcinogenesis"],"prefix":"10.1111","volume":"16","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-4120-0557","authenticated-orcid":false,"given":"Ayaz","family":"Shahid","sequence":"first","affiliation":[{"name":"Department of Biotechnology and Pharmaceutical Sciences College of Pharmacy, Western University of Health Sciences  Pomona California 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