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dc.contributor.authorGirnius, Nomeda A.
dc.contributor.authorEdwards, Yvonne J. K.
dc.contributor.authorGarlick, David S.
dc.contributor.authorDavis, Roger J.
dc.date2022-08-11T08:08:23.000
dc.date.accessioned2022-08-23T15:53:27Z
dc.date.available2022-08-23T15:53:27Z
dc.date.issued2018-06-01
dc.date.submitted2018-07-06
dc.identifier.citation<p>Elife. 2018 Jun 1;7. pii: 36389. doi: 10.7554/eLife.36389. <a href="https://doi.org/10.7554/eLife.36389">Link to article on publisher's site</a></p>
dc.identifier.issn2050-084X (Linking)
dc.identifier.doi10.7554/eLife.36389
dc.identifier.pmid29856313
dc.identifier.urihttp://hdl.handle.net/20.500.14038/29357
dc.description.abstractBreast cancer is the most commonly diagnosed malignancy in women. Analysis of breast cancer genomic DNA indicates frequent loss-of-function mutations in components of the cJUN NH2-terminal kinase (JNK) signaling pathway. Since JNK signaling can promote cell proliferation by activating the AP1 transcription factor, this apparent association of reduced JNK signaling with tumor development was unexpected. We examined the effect of JNK deficiency in the murine breast epithelium. Loss of JNK signaling caused genomic instability and the development of breast cancer. Moreover, JNK deficiency caused widespread early neoplasia and rapid tumor formation in a murine model of breast cancer. This tumor suppressive function was not mediated by a role of JNK in the growth of established tumors, but by a requirement of JNK to prevent tumor initiation. Together, these data identify JNK pathway defects as 'driver' mutations that promote genome instability and tumor initiation.
dc.language.isoen_US
dc.relation<p><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=29856313&dopt=Abstract">Link to Article in PubMed</a></p>
dc.rightsCopyright: © 2018, Girnius et al. This article is distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use and redistribution provided that the original author and source are credited.
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/
dc.subjectJNK
dc.subjectbreast cancer
dc.subjectcancer biology
dc.subjectcell biology
dc.subjectmouse
dc.subjectstress-activated MAPK
dc.subjectBiochemistry, Biophysics, and Structural Biology
dc.subjectCell and Developmental Biology
dc.subjectCellular and Molecular Physiology
dc.subjectEnzymes and Coenzymes
dc.subjectGenetic Phenomena
dc.subjectNeoplasms
dc.titleThe cJUN NH2-terminal kinase (JNK) signaling pathway promotes genome stability and prevents tumor initiation
dc.typeJournal Article
dc.source.journaltitleeLife
dc.source.volume7
dc.identifier.legacyfulltexthttps://escholarship.umassmed.edu/cgi/viewcontent.cgi?article=2594&amp;context=faculty_pubs&amp;unstamped=1
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/faculty_pubs/1584
dc.identifier.contextkey12450403
refterms.dateFOA2022-08-23T15:53:27Z
html.description.abstract<p>Breast cancer is the most commonly diagnosed malignancy in women. Analysis of breast cancer genomic DNA indicates frequent loss-of-function mutations in components of the cJUN NH2-terminal kinase (JNK) signaling pathway. Since JNK signaling can promote cell proliferation by activating the AP1 transcription factor, this apparent association of reduced JNK signaling with tumor development was unexpected. We examined the effect of JNK deficiency in the murine breast epithelium. Loss of JNK signaling caused genomic instability and the development of breast cancer. Moreover, JNK deficiency caused widespread early neoplasia and rapid tumor formation in a murine model of breast cancer. This tumor suppressive function was not mediated by a role of JNK in the growth of established tumors, but by a requirement of JNK to prevent tumor initiation. Together, these data identify JNK pathway defects as 'driver' mutations that promote genome instability and tumor initiation.</p>
dc.identifier.submissionpathfaculty_pubs/1584
dc.contributor.departmentProgram in Molecular Medicine
dc.source.pagese36389


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Copyright: © 2018, Girnius et al. This article is distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use and redistribution provided that the original author and source are credited.
Except where otherwise noted, this item's license is described as Copyright: © 2018, Girnius et al. This article is distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use and redistribution provided that the original author and source are credited.