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Article: Long-term expression of angiostatin suppresses metastatic liver cancer in mice

TitleLong-term expression of angiostatin suppresses metastatic liver cancer in mice
Authors
Issue Date2003
PublisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www.hepatology.org/
Citation
Hepatology, 2003, v. 37 n. 6, p. 1451-1460 How to Cite?
AbstractMetastatic liver cancer has a very poor prognosis and lacks effective therapy. Anti-angiogenic therapies, which starve tumors of blood supply, have proven to be effective in preclinical models because tumor growth is angiogenesis dependent. However, long-term, high-level, and sustained expression of angiogenesis inhibitors, such as angiostatin, is necessary to prevent dormant tumors from becoming active again. To achieve this objective, we engineered a recombinant adeno-associated virus (AAV) vector encoding mouse angiostatin, an endogenous inhibitor of tumor vascularization. After intraportal delivery of this vector, high-level, stable transgene expression of angiostatin lasting for at least 6 months was observed locally in hepatocytes. Gene transfer of AAV-angiostatin via the portal vein led to significant suppression of the growth of both nodular and metastatic EL-4 lymphoma tumors established in the liver and prolonged the survival time of the mice. The growth of neovessels was inhibited significantly, and extensive apoptosis of tumor cells was observed. The anti-angiogenic activity of angiostatin was independent of vascular endothelial growth factor (VEGF). The AAV-angiostatin viruses did not appear to be toxic to mice, and there was no detectable apoptosis of hepatocytes. In conclusion, these encouraging results warrant future investigation of the use of AAV-mediated anti-angiogenic gene therapy for targeting unresectable liver metastases, especially after surgical removal of primary tumors.
Persistent Identifierhttp://hdl.handle.net/10722/84053
ISSN
2015 Impact Factor: 11.711
2015 SCImago Journal Rankings: 4.752
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorXu, Ren_HK
dc.contributor.authorSun, Xen_HK
dc.contributor.authorTse, LYen_HK
dc.contributor.authorLi, Hen_HK
dc.contributor.authorChan, PCen_HK
dc.contributor.authorXu, Sen_HK
dc.contributor.authorXiao, Wen_HK
dc.contributor.authorKung, HFen_HK
dc.contributor.authorKrissansen, GWen_HK
dc.contributor.authorFan, STen_HK
dc.date.accessioned2010-09-06T08:48:22Z-
dc.date.available2010-09-06T08:48:22Z-
dc.date.issued2003en_HK
dc.identifier.citationHepatology, 2003, v. 37 n. 6, p. 1451-1460en_HK
dc.identifier.issn0270-9139en_HK
dc.identifier.urihttp://hdl.handle.net/10722/84053-
dc.description.abstractMetastatic liver cancer has a very poor prognosis and lacks effective therapy. Anti-angiogenic therapies, which starve tumors of blood supply, have proven to be effective in preclinical models because tumor growth is angiogenesis dependent. However, long-term, high-level, and sustained expression of angiogenesis inhibitors, such as angiostatin, is necessary to prevent dormant tumors from becoming active again. To achieve this objective, we engineered a recombinant adeno-associated virus (AAV) vector encoding mouse angiostatin, an endogenous inhibitor of tumor vascularization. After intraportal delivery of this vector, high-level, stable transgene expression of angiostatin lasting for at least 6 months was observed locally in hepatocytes. Gene transfer of AAV-angiostatin via the portal vein led to significant suppression of the growth of both nodular and metastatic EL-4 lymphoma tumors established in the liver and prolonged the survival time of the mice. The growth of neovessels was inhibited significantly, and extensive apoptosis of tumor cells was observed. The anti-angiogenic activity of angiostatin was independent of vascular endothelial growth factor (VEGF). The AAV-angiostatin viruses did not appear to be toxic to mice, and there was no detectable apoptosis of hepatocytes. In conclusion, these encouraging results warrant future investigation of the use of AAV-mediated anti-angiogenic gene therapy for targeting unresectable liver metastases, especially after surgical removal of primary tumors.en_HK
dc.languageengen_HK
dc.publisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www.hepatology.org/en_HK
dc.relation.ispartofHepatologyen_HK
dc.rightsHepatology. Copyright © John Wiley & Sons, Inc.en_HK
dc.titleLong-term expression of angiostatin suppresses metastatic liver cancer in miceen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0270-9139&volume=37&issue=6&spage=1451&epage=1460&date=2003&atitle=Long-term+expression+of+angiostatin+suppresses+metastatic+liver+cancer+in+miceen_HK
dc.identifier.emailFan, ST: stfan@hku.hken_HK
dc.identifier.authorityFan, ST=rp00355en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1053/jhep.2003.50244en_HK
dc.identifier.pmid12774025-
dc.identifier.scopuseid_2-s2.0-0038580344en_HK
dc.identifier.hkuros79082en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0038580344&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume37en_HK
dc.identifier.issue6en_HK
dc.identifier.spage1451en_HK
dc.identifier.epage1460en_HK
dc.identifier.isiWOS:000183236700029-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridXu, R=7402813857en_HK
dc.identifier.scopusauthoridSun, X=8599707500en_HK
dc.identifier.scopusauthoridTse, LY=36891045500en_HK
dc.identifier.scopusauthoridLi, H=36078286800en_HK
dc.identifier.scopusauthoridChan, PC=36944293400en_HK
dc.identifier.scopusauthoridXu, S=7404439649en_HK
dc.identifier.scopusauthoridXiao, W=7202456485en_HK
dc.identifier.scopusauthoridKung, HF=7402514190en_HK
dc.identifier.scopusauthoridKrissansen, GW=7004770042en_HK
dc.identifier.scopusauthoridFan, ST=7402678224en_HK

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