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Breaking the NF-kB and STAT3 Alliance Inhibits Inflammation and Pancreatic Tumorigenesis

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dc.contributor.authorSurh, Young-Joon-
dc.contributor.authorBode, Ann M.-
dc.contributor.authorDong, Zigang-
dc.date.accessioned2021-01-31T09:24:42Z-
dc.date.available2021-01-31T09:24:42Z-
dc.date.issued2010-11-
dc.identifier.citationCancer Prevention Research, Vol.3 No.11, pp.1379-1381-
dc.identifier.issn1940-6207-
dc.identifier.other2478-
dc.identifier.urihttps://hdl.handle.net/10371/172651-
dc.description.abstractThis perspective on Liby et al. (beginning on page 1427 in this issue of the journal) discusses the importance of the finding that two synthetic triterpenoids prolonged survival in a pancreatic cancer mouse model. This finding is significant because pancreatic cancer is one of the deadliest human cancers. These compounds inhibited the interaction between NF-kappa B and signal transducer and activator of transcription 3, and determining the mechanisms underlying this inhibition will help to rapidly move these compounds into phase I clinical trials. Cancer Prev Res; 3(11); 1379-81. (C) 2010 AACR.-
dc.titleBreaking the NF-kB and STAT3 Alliance Inhibits Inflammation and Pancreatic Tumorigenesis-
dc.typeArticle-
dc.contributor.AlternativeAuthor서영준-
dc.identifier.doi10.1158/1940-6207.CAPR-10-0251-
dc.citation.journaltitleCancer Prevention Research-
dc.identifier.scopusid2-s2.0-78649235589-
dc.citation.endpage1381-
dc.citation.number11-
dc.citation.startpage1379-
dc.citation.volume3-
dc.identifier.urlhttps://cancerpreventionresearch.aacrjournals.org/content/3/11/1379.full-text.pdf-
dc.identifier.rimsid2478-
dc.identifier.sci000283991400005-
dc.contributor.affiliatedAuthorSurh, Young-Joon-
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Graduate School of Convergence Science and Technology (융합과학기술대학원)Dept. of Molecular and Biopharmaceutical Sciences (분자의학 및 바이오제약학과)Journal Papers (저널논문_분자의학 및 바이오제약학과)
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