Identification of novel metastasis suppressor signaling pathways for breast cancer

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dc.contributor.authorA J Minn-
dc.contributor.authorE Bevilacqua-
dc.contributor.authorJi Eun Yun-
dc.contributor.authorM R Rosner-
dc.date.accessioned2017-04-19T09:32:09Z-
dc.date.available2017-04-19T09:32:09Z-
dc.date.issued2012-
dc.identifier.issn1538-4101-
dc.identifier.uri10.4161/cc.20624ko
dc.identifier.urihttps://oak.kribb.re.kr/handle/201005/10799-
dc.description.abstractCancer lethality is mainly caused by metastasis. Therefore, understanding the nature of the genes involved in this process has become a priority. Given the heterogeneity of mutations in cancer cells, considerable focus has been directed toward characterizing metastasis genes in the context of relevant signaling pathways rather than treating genes as independent and equal entities. One signaling cascade implicated in the regulation of cell growth, invasion and metastasis is the MAP kinase pathway. Raf kinase inhibitory protein (RKIP) functions as an inhibitor of the MAP kinase pathway and is a metastasis suppressor in different cancer models. By utilizing statistical analysis of clinical data integrated with experimental validation, we recently identified components of the RKIP signaling pathway relevant to breast cancer metastasis. Using the RKIP pathway as an example, we show how prior biological knowledge can be efficiently combined with genome-wide patient data to identify gene regulatory mechanisms that control metastasis.-
dc.publisherT&F (Taylor & Francis)-
dc.titleIdentification of novel metastasis suppressor signaling pathways for breast cancer-
dc.title.alternativeIdentification of novel metastasis suppressor signaling pathways for breast cancer-
dc.typeArticle-
dc.citation.titleCell Cycle-
dc.citation.number13-
dc.citation.endPage2457-
dc.citation.startPage2452-
dc.citation.volume11-
dc.contributor.affiliatedAuthorJi Eun Yun-
dc.contributor.alternativeNameMinn-
dc.contributor.alternativeNameBevilacqua-
dc.contributor.alternativeName윤지은-
dc.contributor.alternativeNameRosner-
dc.identifier.bibliographicCitationCell Cycle, vol. 11, no. 13, pp. 2452-2457-
dc.identifier.doi10.4161/cc.20624-
dc.subject.keywordBreast cancer-
dc.subject.keywordGene set analysis-
dc.subject.keywordGene set enrichment analysis-
dc.subject.keywordGene signature-
dc.subject.keywordInvasion-
dc.subject.keywordMetastasis-
dc.subject.keywordRaf kinase inhibitory protein-
dc.subject.keywordRandom forests-
dc.subject.keywordSignaling pathway-
dc.subject.localbreast cancer-
dc.subject.localBreast cancer-
dc.subject.localBreast Cancer-
dc.subject.localGene set analysis-
dc.subject.localGene set enrichment analysis-
dc.subject.localGene set enrichment analysis (GSEA)-
dc.subject.localGene signature-
dc.subject.localgene signature-
dc.subject.localinvasion-
dc.subject.localInvasion-
dc.subject.localmetastasis-
dc.subject.localMetastasis-
dc.subject.localRaf kinase inhibitory protein-
dc.subject.localRandom forest-
dc.subject.localrandom forest-
dc.subject.localRandom forests-
dc.subject.localRandom Forest-
dc.subject.localSignaling pathways-
dc.subject.localsignaling pathways-
dc.subject.localSignaling pathway-
dc.description.journalClassY-
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