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dc.contributor.authorGoel, Hira Lal
dc.contributor.authorAlam, Naved
dc.contributor.authorJohnson, Isaac N.S.
dc.contributor.authorLanguino, Lucia R.
dc.date2022-08-11T08:09:39.000
dc.date.accessioned2022-08-23T16:38:38Z
dc.date.available2022-08-23T16:38:38Z
dc.date.issued2009-12-04
dc.date.submitted2010-03-26
dc.identifier.citation<p>Am J Transl Res. 2009 Apr 20;1(3):211-20.</p>
dc.identifier.issn1943-8141 (Electronic)
dc.identifier.pmid19956432
dc.identifier.urihttp://hdl.handle.net/20.500.14038/39289
dc.description.abstractIntegrins are cell surface receptors for extracellular matrix proteins and play a key role in cell survival, proliferation, migration and gene expression. Integrin signaling has been shown to be deregulated in several types of cancer, including prostate cancer. This review is focused on integrin signaling pathways known to be deregulated in prostate cancer and known to promote prostate cancer progression.
dc.language.isoen_US
dc.relation<p><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=19956432&dopt=Abstract">Link to Article in PubMed</a></p>
dc.relation.urlhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC2757165/
dc.subjectLife Sciences
dc.subjectMedicine and Health Sciences
dc.titleIntegrin signaling aberrations in prostate cancer
dc.typeJournal Article
dc.source.journaltitleAmerican journal of translational research
dc.source.volume1
dc.source.issue3
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/oapubs/2089
dc.identifier.contextkey1246891
html.description.abstract<p>Integrins are cell surface receptors for extracellular matrix proteins and play a key role in cell survival, proliferation, migration and gene expression. Integrin signaling has been shown to be deregulated in several types of cancer, including prostate cancer. This review is focused on integrin signaling pathways known to be deregulated in prostate cancer and known to promote prostate cancer progression.</p>
dc.identifier.submissionpathoapubs/2089
dc.contributor.departmentDepartment of Cancer Biology
dc.source.pages211-20


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