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dc.contributor.authorAltieri, Dario C.
dc.contributor.authorLanguino, Lucia R.
dc.contributor.authorLian, Jane B.
dc.contributor.authorStein, Janet L.
dc.contributor.authorLeav, Irwin
dc.contributor.authorVan Wijnen, Andre J.
dc.contributor.authorJiang, Zhong
dc.contributor.authorStein, Gary S.
dc.date2022-08-11T08:10:57.000
dc.date.accessioned2022-08-23T17:26:17Z
dc.date.available2022-08-23T17:26:17Z
dc.date.issued2009-08-06
dc.date.submitted2011-01-11
dc.identifier.citationJ Cell Biochem. 2009 Aug 1;107(5):845-52. <a href="http://dx.doi.org/10.1002/jcb.22162">Link to article on publisher's site</a>
dc.identifier.issn0730-2312 (Linking)
dc.identifier.doi10.1002/jcb.22162
dc.identifier.pmid19492418
dc.identifier.urihttp://hdl.handle.net/20.500.14038/49605
dc.description.abstractAlthough the timing with which common epithelial malignancies arise and become established remains a matter of debate, it is clear that by the time they are detected these tumors harbor hundreds of deregulated, aberrantly expressed or mutated genes. This enormous complexity poses formidable challenges to identify gene pathways that are drivers of tumorigenesis, potentially suitable for therapeutic intervention. An alternative approach is to consider cancer pathways as interconnected networks, and search for potential nodal proteins capable of connecting multiple signaling networks of tumor maintenance. We have modeled this approach in advanced prostate cancer, a condition with current limited therapeutic options. We propose that the integration of three signaling networks, including chaperone-mediated mitochondrial homeostasis, integrin-dependent cell signaling, and Runx2-regulated gene expression in the metastatic bone microenvironment plays a critical role in prostate cancer maintenance, and offers novel options for molecular therapy.
dc.language.isoen_US
dc.relation<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=19492418&dopt=Abstract">Link to Article in PubMed</a>
dc.relation.urlhttp://dx.doi.org/10.1002/jcb.22162
dc.subjectDrug Discovery
dc.subject*Gene Expression Regulation, Neoplastic
dc.subject*Gene Regulatory Networks
dc.subjectHumans
dc.subjectIntegrin alphaV
dc.subjectMale
dc.subjectMitochondria
dc.subjectProstatic Neoplasms
dc.subjectSignal Transduction
dc.subjectCell Biology
dc.titleProstate cancer regulatory networks
dc.typeJournal Article
dc.source.journaltitleJournal of cellular biochemistry
dc.source.volume107
dc.source.issue5
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/stein/34
dc.identifier.contextkey1724074
html.description.abstract<p>Although the timing with which common epithelial malignancies arise and become established remains a matter of debate, it is clear that by the time they are detected these tumors harbor hundreds of deregulated, aberrantly expressed or mutated genes. This enormous complexity poses formidable challenges to identify gene pathways that are drivers of tumorigenesis, potentially suitable for therapeutic intervention. An alternative approach is to consider cancer pathways as interconnected networks, and search for potential nodal proteins capable of connecting multiple signaling networks of tumor maintenance. We have modeled this approach in advanced prostate cancer, a condition with current limited therapeutic options. We propose that the integration of three signaling networks, including chaperone-mediated mitochondrial homeostasis, integrin-dependent cell signaling, and Runx2-regulated gene expression in the metastatic bone microenvironment plays a critical role in prostate cancer maintenance, and offers novel options for molecular therapy.</p>
dc.identifier.submissionpathstein/34
dc.contributor.departmentDepartment of Cell Biology
dc.contributor.departmentDepartment of Pathology
dc.contributor.departmentDepartment of Cancer Biology
dc.source.pages845-52


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