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dc.contributor.authorMercurio, Arthur M.
dc.contributor.authorBachelder, Robin E.
dc.contributor.authorBates, Richard C.
dc.contributor.authorChung, Jun
dc.date2022-08-11T08:08:02.000
dc.date.accessioned2022-08-23T15:39:48Z
dc.date.available2022-08-23T15:39:48Z
dc.date.issued2004-03-17
dc.date.submitted2010-11-07
dc.identifier.citationSemin Cancer Biol. 2004 Apr;14(2):115-22. <a href="http://dx.doi.org/10.1016/j.semcancer.2003.09.016">Link to article on publisher's site</a>
dc.identifier.issn1044-579X (Linking)
dc.identifier.doi10.1016/j.semcancer.2003.09.016
dc.identifier.pmid15018895
dc.identifier.urihttp://hdl.handle.net/20.500.14038/26255
dc.description.abstractThis review highlights an emerging function for vascular endothelial growth factor (VEGF) in carcinoma and discusses mechanisms involved in the elaboration of VEGF autocrine loops. Evidence is provided that autocrine VEGF contributes to the two major components of invasive carcinoma: survival and migration. Moreover, the findings discussed support the hypothesis that carcinoma progression selects for cells that depend on VEGF as a survival factor. Furthermore, a related hypothesis, which is developed, is that the function of the alpha6beta4 integrin, which has been implicated in carcinoma progression, is linked to its ability to regulate VEGF translation and, consequently, autocrine VEGF signaling. The findings reviewed challenge the notion that the function of VEGF in cancer is limited to angiogenesis and suggest that VEGF and VEGF receptor-based therapeutics, in addition to targeting angiogenesis, may also impair tumor cell survival and invasion directly.
dc.language.isoen_US
dc.relation<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=15018895&dopt=Abstract">Link to Article in PubMed</a>
dc.relation.urlhttp://dx.doi.org/10.1016/j.semcancer.2003.09.016
dc.subject*Autocrine Communication
dc.subjectCarcinoma
dc.subjectHumans
dc.subjectIntegrin alpha6beta4
dc.subjectSignal Transduction
dc.subjectVascular Endothelial Growth Factor A
dc.subjectCancer Biology
dc.subjectNeoplasms
dc.titleAutocrine signaling in carcinoma: VEGF and the alpha6beta4 integrin
dc.typeJournal Article
dc.source.journaltitleSeminars in cancer biology
dc.source.volume14
dc.source.issue2
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/cancerbiology_pp/169
dc.identifier.contextkey1633394
html.description.abstract<p>This review highlights an emerging function for vascular endothelial growth factor (VEGF) in carcinoma and discusses mechanisms involved in the elaboration of VEGF autocrine loops. Evidence is provided that autocrine VEGF contributes to the two major components of invasive carcinoma: survival and migration. Moreover, the findings discussed support the hypothesis that carcinoma progression selects for cells that depend on VEGF as a survival factor. Furthermore, a related hypothesis, which is developed, is that the function of the alpha6beta4 integrin, which has been implicated in carcinoma progression, is linked to its ability to regulate VEGF translation and, consequently, autocrine VEGF signaling. The findings reviewed challenge the notion that the function of VEGF in cancer is limited to angiogenesis and suggest that VEGF and VEGF receptor-based therapeutics, in addition to targeting angiogenesis, may also impair tumor cell survival and invasion directly.</p>
dc.identifier.submissionpathcancerbiology_pp/169
dc.contributor.departmentDepartment of Cancer Biology
dc.source.pages115-22


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