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dc.contributor.authorGuha, Minakshi
dc.contributor.authorAltieri, Dario C.
dc.date2022-08-11T08:09:39.000
dc.date.accessioned2022-08-23T16:38:44Z
dc.date.available2022-08-23T16:38:44Z
dc.date.issued2009-09-01
dc.date.submitted2010-03-29
dc.identifier.citationCell Cycle. 2009 Sep 1;8(17):2708-10. Epub 2009 Sep 7. <a href="http://dx.doi.org/10.4161/cc.8.17.9457">Link to article on publisher's website</a>
dc.identifier.issn1551-4005 (Linking)
dc.identifier.doi10.4161/cc.8.17.9457
dc.identifier.pmid19717980
dc.identifier.urihttp://hdl.handle.net/20.500.14038/39313
dc.description<p>Co-author Minakshi Guha is a student in the Cancer Biology program in the Graduate School of Biomedical Sciences (GSBS) at UMass Medical School.</p>
dc.description.abstractDespite the constant exposure to genomic insults that may lead to malignancy, cancer is surprisingly a relatively rare occurrence, and this is largely credited to an elaborate network of endogenous tumor suppression. Many effectors of tumor suppression have been identified, and their functions when activated in damaged cells have in large part been elucidated. What is less clear is whether there are common target gene(s) of tumor suppression, whose expression must be ablated in order to block transformation and preserve cellular homeostasis. Fresh experimental evidence suggests that silencing of the mitotic regulator and cell death inhibitor, survivin, is a universal requirement for successful tumor suppression in humans.
dc.language.isoen_US
dc.relation<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=19717980&dopt=Abstract">Link to Article in PubMed</a>
dc.relation.urlhttp://www.landesbioscience.com/journals/cc/article/9457/
dc.subjectApoptosis
dc.subjectGene Expression Regulation, Neoplastic
dc.subjectGene Silencing
dc.subjectHumans
dc.subjectMicrotubule-Associated Proteins
dc.subjectPTEN Phosphohydrolase
dc.subjectTumor Suppressor Proteins
dc.subjectCancer Biology
dc.subjectLife Sciences
dc.subjectMedicine and Health Sciences
dc.titleSurvivin as a global target of intrinsic tumor suppression networks
dc.typeJournal Article
dc.source.journaltitleCell cycle (Georgetown, Tex.)
dc.source.volume8
dc.source.issue17
dc.identifier.legacyfulltexthttps://escholarship.umassmed.edu/cgi/viewcontent.cgi?article=3112&amp;context=oapubs&amp;unstamped=1
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/oapubs/2113
dc.identifier.contextkey1250243
refterms.dateFOA2022-08-23T16:38:44Z
html.description.abstract<p>Despite the constant exposure to genomic insults that may lead to malignancy, cancer is surprisingly a relatively rare occurrence, and this is largely credited to an elaborate network of endogenous tumor suppression. Many effectors of tumor suppression have been identified, and their functions when activated in damaged cells have in large part been elucidated. What is less clear is whether there are common target gene(s) of tumor suppression, whose expression must be ablated in order to block transformation and preserve cellular homeostasis. Fresh experimental evidence suggests that silencing of the mitotic regulator and cell death inhibitor, survivin, is a universal requirement for successful tumor suppression in humans.</p>
dc.identifier.submissionpathoapubs/2113
dc.contributor.departmentDepartment of Cancer Biology
dc.source.pages2708-10


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