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• W2793670379 startingPage "673" @default.
• W2793670379 abstract "Epidemiologic data clearly shows a correlation between cigarette smoking and pancreatic adenocarcinoma, chronic pancreatitis, and acute pancreatitis. Following exposure to cigarette smoke, several pancreas-specific events occur that contribute to the development of pancreatic adenocarcinoma. The physiologic damage of cigarette smoking begins with the inhalation of inactive carcinogens, followed by their subsequent delivery to end organs and tissues through the vascular system. Following delivery, carcinogens are metabolized to active electrophiles in their target tissues. In pancreatic tissue, it has previously been demonstrated that cigarette smoke-derived carcinogens are metabolized to carcinogenic compounds such as nicotine-derived nitrosamine ketone (NNK). These carcinogens induce a variety of functional cellular alterations by interacting with acetylcholine receptors in pancreatic tissue. While it is known that these alterations contribute to the induction of metaplasia, current evidence for cigarette smoke-induced pancreatic disease remains incomplete." @default.
• W2793670379 created "2018-03-29" @default.
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• W2793670379 date "2018-02-12" @default.
• W2793670379 modified "2023-10-14" @default.
• W2793670379 title "Smoking, a Risk for Pancreatic Cancer" @default.
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• W2793670379 doi "https://doi.org/10.1002/9781119188421.ch89" @default.
• W2793670379 hasPublicationYear "2018" @default.
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