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Conference Paper: Nicotine and gastric cancer

TitleNicotine and gastric cancer
Authors
KeywordsExtracellular signal-regulated kinase (ERK)
Cyclooxygenase-2 (COX-2)
Ornithine decarboxylase (ODC)
c-myc
Issue Date2005
Citation
Alcohol, 2005, v. 35, n. 3, p. 259-264 How to Cite?
AbstractAbout 60 components in cigarette smoke are considered to be carcinogens, namely polycyclic aromatic hydrocarbons, nitrosamines, aromatic amine, trace metals, as well as nicotine. Nicotine is considered to be one of the active components in cigarette smoke, and its association with tumorigenesis is enigmatic. Nonsteroidal antiinflammatory drugs are widely accepted as antitumor agents to treat patients with cancer by inhibiting cyclooxygenase-2 activity. Stimulation of tumor growth by nicotine involves different processes of cell proliferation and angiogenesis. Study results, with the use of animal xenograft models and cell culture systems, show that nicotine stimulates the progression of tumor growth, through a cyclooxygenase-2-dependent pathway. On the basis of these findings, nicotine seems to be a potent mitogenic agent in modulating tumor cell proliferation, and selective cyclooxygenase-2 inhibitors are promising antitumor agents for gastric cancer in smokers. © 2005 Elsevier Inc. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/207505
ISSN
2015 Impact Factor: 2.44
2015 SCImago Journal Rankings: 0.922

 

DC FieldValueLanguage
dc.contributor.authorShin, Vivianyvonne-
dc.contributor.authorCho, Chihin-
dc.date.accessioned2014-12-31T01:01:48Z-
dc.date.available2014-12-31T01:01:48Z-
dc.date.issued2005-
dc.identifier.citationAlcohol, 2005, v. 35, n. 3, p. 259-264-
dc.identifier.issn0741-8329-
dc.identifier.urihttp://hdl.handle.net/10722/207505-
dc.description.abstractAbout 60 components in cigarette smoke are considered to be carcinogens, namely polycyclic aromatic hydrocarbons, nitrosamines, aromatic amine, trace metals, as well as nicotine. Nicotine is considered to be one of the active components in cigarette smoke, and its association with tumorigenesis is enigmatic. Nonsteroidal antiinflammatory drugs are widely accepted as antitumor agents to treat patients with cancer by inhibiting cyclooxygenase-2 activity. Stimulation of tumor growth by nicotine involves different processes of cell proliferation and angiogenesis. Study results, with the use of animal xenograft models and cell culture systems, show that nicotine stimulates the progression of tumor growth, through a cyclooxygenase-2-dependent pathway. On the basis of these findings, nicotine seems to be a potent mitogenic agent in modulating tumor cell proliferation, and selective cyclooxygenase-2 inhibitors are promising antitumor agents for gastric cancer in smokers. © 2005 Elsevier Inc. All rights reserved.-
dc.languageeng-
dc.relation.ispartofAlcohol-
dc.subjectExtracellular signal-regulated kinase (ERK)-
dc.subjectCyclooxygenase-2 (COX-2)-
dc.subjectOrnithine decarboxylase (ODC)-
dc.subjectc-myc-
dc.titleNicotine and gastric cancer-
dc.typeConference_Paper-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.alcohol.2005.04.007-
dc.identifier.pmid16054988-
dc.identifier.scopuseid_2-s2.0-23144444556-
dc.identifier.volume35-
dc.identifier.issue3-
dc.identifier.spage259-
dc.identifier.epage264-

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