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dc.contributor.authorImprogo, Ma. Reina D.
dc.contributor.authorScofield, Michael D.
dc.contributor.authorTapper, Andrew R.
dc.contributor.authorGardner, Paul D.
dc.date2022-08-11T08:08:53.000
dc.date.accessioned2022-08-23T16:11:11Z
dc.date.available2022-08-23T16:11:11Z
dc.date.issued2010-06-28
dc.date.submitted2010-09-02
dc.identifier.citation<p>Improgo MRD, Scofield MD, Tapper AR, and Gardner PD. 2010. From Smoking to Lung Cancer: The Nicotinic Receptor Connection. Oncogene 29 (35): 4874-4884. DOI 10.1038/onc.2010.256. <a href="http://dx.doi.org/10.1038/onc.2010.256">Link to article on publisher's website</a></p>
dc.identifier.issn1476-5594
dc.identifier.doi10.1038/onc.2010.256
dc.identifier.pmid20581870
dc.identifier.urihttp://hdl.handle.net/20.500.14038/33108
dc.description.abstractNicotinic acetylcholine receptors (nAChRs) are ligand-gated ion channels that modulate key physiological processes ranging from neurotransmission to cancer signaling. These receptors are activated by the neurotransmitter, acetylcholine, and the tobacco alkaloid, nicotine. Recently, the gene cluster encoding the alpha3, alpha5 and beta4 nAChR subunits received heightened interest after a succession of linkage analyses and association studies identified multiple single-nucleotide polymorphisms in these genes that are associated with an increased risk for nicotine dependence and lung cancer. It is not clear whether the risk for lung cancer is direct or an effect of nicotine dependence, as evidence for both scenarios exist. In this study, we summarize the body of work implicating nAChRs in the pathogenesis of lung cancer, with special focus on the clustered nAChR subunits and their emerging role in this disease state.Oncogene advance online publication, 28 June 2010; doi:10.1038/onc.2010.256.
dc.language.isoen_US
dc.publisherNature Publishing Group
dc.relation<p><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=20581870&dopt=Abstract">Link to article in PubMed</a></p>
dc.relation.urlhttp://dx.doi.org/10.1038/onc.2010.256
dc.subjectReceptors, Nicotinic; Nerve Tissue Proteins; Lung Neoplasms; Tobacco Use Disorder
dc.subjectLife Sciences
dc.subjectMedicine and Health Sciences
dc.subjectNeuroscience and Neurobiology
dc.subjectOncology
dc.subjectPsychiatry
dc.titleFrom smoking to lung cancer: the CHRNA5/A3/B4 connection
dc.typeJournal Article
dc.source.journaltitleOncogene
dc.source.volume29
dc.source.issue35
dc.identifier.legacyfulltexthttps://escholarship.umassmed.edu/cgi/viewcontent.cgi?article=2653&amp;context=gsbs_sp&amp;unstamped=1
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/gsbs_sp/1651
dc.identifier.contextkey1534590
refterms.dateFOA2022-08-23T16:11:12Z
html.description.abstract<p>Nicotinic acetylcholine receptors (nAChRs) are ligand-gated ion channels that modulate key physiological processes ranging from neurotransmission to cancer signaling. These receptors are activated by the neurotransmitter, acetylcholine, and the tobacco alkaloid, nicotine. Recently, the gene cluster encoding the alpha3, alpha5 and beta4 nAChR subunits received heightened interest after a succession of linkage analyses and association studies identified multiple single-nucleotide polymorphisms in these genes that are associated with an increased risk for nicotine dependence and lung cancer. It is not clear whether the risk for lung cancer is direct or an effect of nicotine dependence, as evidence for both scenarios exist. In this study, we summarize the body of work implicating nAChRs in the pathogenesis of lung cancer, with special focus on the clustered nAChR subunits and their emerging role in this disease state.Oncogene advance online publication, 28 June 2010; doi:10.1038/onc.2010.256.</p>
dc.identifier.submissionpathgsbs_sp/1651
dc.contributor.departmentGardner Lab
dc.contributor.departmentTapper Lab
dc.contributor.departmentDepartment of Psychiatry
dc.contributor.departmentBrudnick Neuropsychiatric Research Institute
dc.contributor.departmentGraduate School of Biomedical Sciences, Interdisciplinary Graduate Program
dc.contributor.departmentGraduate School of Biomedical Sciences, Program in Neuroscience
dc.source.pages4874-4884
dc.contributor.studentImprogo, Ma Reina D.; Scofield, Michael D.
dc.description.thesisprogramNeuroscience


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