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Article: VEGF signaling inhibitors: More pro-apoptotic than anti-angiogenic

TitleVEGF signaling inhibitors: More pro-apoptotic than anti-angiogenic
Authors
KeywordsAngiogenesis
Apoptosis
Bevacizumab
Chemosensitization
Permeability
Issue Date2007
PublisherSpringer New York LLC. The Journal's web site is located at http://springerlink.metapress.com/openurl.asp?genre=journal&issn=0167-7659
Citation
Cancer And Metastasis Reviews, 2007, v. 26 n. 3-4, p. 443-452 How to Cite?
AbstractThe vascular endothelial growth factor (VEGF) family of polypeptide growth factors regulates a family of VEGF receptor (VEGFR) tyrosine kinases with pleiotropic downstream effects. Angiogenesis is the best known of these effects, but additional VEGF-dependent actions include increased vascular permeability, paracrine/autocrine growth factor release, enhancement of cell motility, and inhibition of apoptosis. In theory, therapeutic inhibition of angiogenesis should reduce tumor perfusion and thus increase tumor hypoxia and chemoresistance, but in clinical practice the VEGF antibody bevacizumab acts as a broad-spectrum chemosensitizer. Since VEGFR expression occurs in many tumor types, such chemosensitization is more readily explained by direct inhibition of tumor cell survival signals than by indirect stromal/vascular effects. The emerging model of anti-VEGF drug action being mediated primarily by tumoral (as distinct from endothelial) VEGFRs has clinically important implications for optimizing the anti-metastatic efficacy of this expanding drug class. © 2007 Springer Science+Business Media, LLC.
Persistent Identifierhttp://hdl.handle.net/10722/77601
ISSN
2015 Impact Factor: 5.316
2015 SCImago Journal Rankings: 2.801
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorEpstein, RJen_HK
dc.date.accessioned2010-09-06T07:33:40Z-
dc.date.available2010-09-06T07:33:40Z-
dc.date.issued2007en_HK
dc.identifier.citationCancer And Metastasis Reviews, 2007, v. 26 n. 3-4, p. 443-452en_HK
dc.identifier.issn0167-7659en_HK
dc.identifier.urihttp://hdl.handle.net/10722/77601-
dc.description.abstractThe vascular endothelial growth factor (VEGF) family of polypeptide growth factors regulates a family of VEGF receptor (VEGFR) tyrosine kinases with pleiotropic downstream effects. Angiogenesis is the best known of these effects, but additional VEGF-dependent actions include increased vascular permeability, paracrine/autocrine growth factor release, enhancement of cell motility, and inhibition of apoptosis. In theory, therapeutic inhibition of angiogenesis should reduce tumor perfusion and thus increase tumor hypoxia and chemoresistance, but in clinical practice the VEGF antibody bevacizumab acts as a broad-spectrum chemosensitizer. Since VEGFR expression occurs in many tumor types, such chemosensitization is more readily explained by direct inhibition of tumor cell survival signals than by indirect stromal/vascular effects. The emerging model of anti-VEGF drug action being mediated primarily by tumoral (as distinct from endothelial) VEGFRs has clinically important implications for optimizing the anti-metastatic efficacy of this expanding drug class. © 2007 Springer Science+Business Media, LLC.en_HK
dc.languageengen_HK
dc.publisherSpringer New York LLC. The Journal's web site is located at http://springerlink.metapress.com/openurl.asp?genre=journal&issn=0167-7659en_HK
dc.relation.ispartofCancer and Metastasis Reviewsen_HK
dc.subjectAngiogenesisen_HK
dc.subjectApoptosisen_HK
dc.subjectBevacizumaben_HK
dc.subjectChemosensitizationen_HK
dc.subjectPermeabilityen_HK
dc.titleVEGF signaling inhibitors: More pro-apoptotic than anti-angiogenicen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0167-7659&volume=26&spage=443&epage=52&date=2007&atitle=VEGF+signaling+inhibitors:+More+pro-apoptotic+than+anti-angiogenicen_HK
dc.identifier.emailEpstein, RJ: repstein@hku.hken_HK
dc.identifier.authorityEpstein, RJ=rp00501en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1007/s10555-007-9071-1en_HK
dc.identifier.pmid17786538-
dc.identifier.scopuseid_2-s2.0-36148950966en_HK
dc.identifier.hkuros140621en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-36148950966&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume26en_HK
dc.identifier.issue3-4en_HK
dc.identifier.spage443en_HK
dc.identifier.epage452en_HK
dc.identifier.isiWOS:000250879600008-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridEpstein, RJ=34975074500en_HK
dc.identifier.citeulike1948726-

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