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Cancers 2015, 7(2), 723-735; doi:10.3390/cancers7020723

Pathologic Cellular Events in Smoking-Related Pancreatitis

1
Department of Internal Medicine, Section of Digestive Diseases, Yale University School of Medicine, New Haven, CT 06520, USA
2
Veterans Affairs Connecticut Healthcare, West Haven, CT 06516, USA 
Academic Editor: Hildegard Schuller
Received: 7 April 2015 / Revised: 17 April 2015 / Accepted: 21 April 2015 / Published: 29 April 2015
View Full-Text   |   Download PDF [537 KB, uploaded 29 April 2015]   |  

Abstract

Pancreatitis, a debilitating inflammatory disorder, results from pancreatic injury. Alcohol abuse is the foremost cause, although cigarette smoking has recently surfaced as a distinct risk factor. The mechanisms by which cigarette smoke and its toxins initiate pathological cellular events leading to pancreatitis, have not been clearly defined. Although cigarette smoke is composed of more than 4000 compounds, it is mainly nicotine and the tobacco-specific nitrosamine 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK), which have been extensively studied with respect to pancreatic diseases. This review summarizes these research findings and highlights cellular pathways which may be of relevance in initiation and progression of smoking-related pancreatitis. View Full-Text
Keywords: pancreatitis; smoking; nicotine; 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK); nicotinic acetylcholine receptors (nAChRs); inflammation; bioactivation; β-adrenergic receptors pancreatitis; smoking; nicotine; 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK); nicotinic acetylcholine receptors (nAChRs); inflammation; bioactivation; β-adrenergic receptors
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).

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Thrower, E. Pathologic Cellular Events in Smoking-Related Pancreatitis. Cancers 2015, 7, 723-735.

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