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Article: Deletion of laminin-8 results in increased tumor neovascularization and metastasis in mice

TitleDeletion of laminin-8 results in increased tumor neovascularization and metastasis in mice
Authors
Zhou, ZDoi, MWang, JCao, RLiu, BChan, KMKortesmaa, JSorokin, LCao, YTryggvason, K
Issue Date2004
PublisherAmerican Association for Cancer Research. The Journal's web site is located at http://cancerres.aacrjournals.org/
Citation
Cancer Research, 2004, v. 64 n. 12, p. 4059-4063 How to Cite?
DOI: http://dx.doi.org/10.1158/0008-5472.CAN-04-0291
AbstractLaminin-8 (α4β1γ1) is one of the major laminin isoforms expressed in vascular endothelial basement membranes. Here we show that deletion of laminin-8 in mice affects angiogenesis under pathological conditions. Murine tumor models used in laminin α4-deficient mice results in hyperneovascularization and significant promotion of tumor growth and metastasis. The higher tumor growth rates in mutant mice correlate with decreased tumor cell apoptosis. Depletion of laminin α4 chain may alter the structure of vascular basement membranes, leading to increased angiogenesis. Our data suggest that the laminin-8 plays a critical role in the regulation of pathological angiogenesis.
Persistent Identifierhttp://hdl.handle.net/10722/134123
ISSN
0008-5472
2023 Impact Factor: 12.5
2023 SCImago Journal Rankings: 3.468
ISI Accession Number ID
WOS:000222077900001
References
References in Scopus

 

DC FieldValueLanguage
dc.contributor.authorZhou, Zen_HK
dc.contributor.authorDoi, Men_HK
dc.contributor.authorWang, Jen_HK
dc.contributor.authorCao, Ren_HK
dc.contributor.authorLiu, Ben_HK
dc.contributor.authorChan, KMen_HK
dc.contributor.authorKortesmaa, Jen_HK
dc.contributor.authorSorokin, Len_HK
dc.contributor.authorCao, Yen_HK
dc.contributor.authorTryggvason, Ken_HK
dc.date.accessioned2011-06-13T07:19:37Z-
dc.date.available2011-06-13T07:19:37Z-
dc.date.issued2004en_HK
dc.identifier.citationCancer Research, 2004, v. 64 n. 12, p. 4059-4063en_HK
dc.identifier.issn0008-5472en_HK
dc.identifier.urihttp://hdl.handle.net/10722/134123-
dc.description.abstractLaminin-8 (α4β1γ1) is one of the major laminin isoforms expressed in vascular endothelial basement membranes. Here we show that deletion of laminin-8 in mice affects angiogenesis under pathological conditions. Murine tumor models used in laminin α4-deficient mice results in hyperneovascularization and significant promotion of tumor growth and metastasis. The higher tumor growth rates in mutant mice correlate with decreased tumor cell apoptosis. Depletion of laminin α4 chain may alter the structure of vascular basement membranes, leading to increased angiogenesis. Our data suggest that the laminin-8 plays a critical role in the regulation of pathological angiogenesis.en_HK
dc.languageengen_US
dc.publisherAmerican Association for Cancer Research. The Journal's web site is located at http://cancerres.aacrjournals.org/en_HK
dc.relation.ispartofCancer Researchen_HK
dc.subject.meshAnimalsen_HK
dc.subject.meshCarcinoma, Lewis Lung - blood supply - metabolism - pathologyen_HK
dc.subject.meshCell Division - physiologyen_HK
dc.subject.meshLaminin - biosynthesis - deficiency - geneticsen_HK
dc.subject.meshMelanoma, Experimental - blood supply - metabolism - pathologyen_HK
dc.subject.meshMiceen_HK
dc.subject.meshMice, Inbred C57BLen_HK
dc.subject.meshNeoplasm Metastasisen_HK
dc.subject.meshNeovascularization, Pathologic - genetics - metabolism - pathologyen_HK
dc.titleDeletion of laminin-8 results in increased tumor neovascularization and metastasis in miceen_HK
dc.typeArticleen_HK
dc.identifier.emailZhou, Z: zhongjun@hkucc.hku.hken_HK
dc.identifier.emailLiu, B: ppliew@hku.hken_HK
dc.identifier.emailChan, KM: ming616@graduate.hku.hken_HK
dc.identifier.authorityZhou, Z=rp00503en_HK
dc.identifier.authorityLiu, B=rp01485en_HK
dc.identifier.authorityChan, KM=rp01757en_HK
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1158/0008-5472.CAN-04-0291en_HK
dc.identifier.pmid15205311-
dc.identifier.scopuseid_2-s2.0-3042663099en_HK
dc.identifier.hkuros97919-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-3042663099&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume64en_HK
dc.identifier.issue12en_HK
dc.identifier.spage4059en_HK
dc.identifier.epage4063en_HK
dc.identifier.isiWOS:000222077900001-
dc.publisher.placeUnited Statesen_HK
dc.identifier.f10001020090-
dc.identifier.scopusauthoridZhou, Z=8631856300en_HK
dc.identifier.scopusauthoridDoi, M=35811992500en_HK
dc.identifier.scopusauthoridWang, J=8631854400en_HK
dc.identifier.scopusauthoridCao, R=7103341338en_HK
dc.identifier.scopusauthoridLiu, B=7408693394en_HK
dc.identifier.scopusauthoridChan, KM=8631854500en_HK
dc.identifier.scopusauthoridKortesmaa, J=6603087164en_HK
dc.identifier.scopusauthoridSorokin, L=35467632200en_HK
dc.identifier.scopusauthoridCao, Y=7404524342en_HK
dc.identifier.scopusauthoridTryggvason, K=7102025185en_HK
dc.identifier.issnl0008-5472-

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