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Article: Microvessel density, vascular endothelial growth factor and its receptors Flt-1 and Flk-1/KDR in hepatocellular carcinoma

TitleMicrovessel density, vascular endothelial growth factor and its receptors Flt-1 and Flk-1/KDR in hepatocellular carcinoma
Authors
KeywordsFlk-1/KDR
Flt-1
Hepatocellular carcinoma
Microvessel density
Vascular endothelial growth factor
VEGF
Issue Date2001
PublisherAmerican Society for Clinical Pathology. The Journal's web site is located at http://www.ajcp.com
Citation
American Journal Of Clinical Pathology, 2001, v. 116 n. 6, p. 838-845 How to Cite?
AbstractAssessment of angiogenesis may yield important information for an effective antiangiogenic treatment for hepatocellular carcinoma (HCC) because HCC is characteristically hypervascular. We examined the relationship of microvessel density (MVD), vascular endothelial growth factor (VEGF), and VEGF receptors Flt-1 and Flk-1/KDR in 50 patients with HCC and in 3 hepatoma cell lines. VEGF messenger RNA (mRNA) was overexpressed in 26 tumors (52%), and the 3 VEGF isoforms (121, 165, and 189) were present in high frequencies. Flt-1 mRNA was overexpressed in 34 tumors (68%), with levels significantly increased in HCCs compared with the nontumorous livers. Tumor Flt-1 mRNA significantly correlated with tumor VEGF mRNA levels. Within the group of tumors 8.5 cm or less in diameter, tumors with intrahepatic metastasis in the form of tumor microsatellite formation had significantly higher VEGF mRNA levels. MVD assessed by immunohistochemical analysis with CD34 antibody was inversely related to tumor size. Angiogenesis as assessed by MVD and tumor VEGF expression seems to have a more important role in tumor growth and intrahepatic metastasis in smaller HCCs. The differential up-regulation of Flt-1 suggests that it may have an important role in angiogenesis in HCC.
Persistent Identifierhttp://hdl.handle.net/10722/88657
ISSN
2015 Impact Factor: 2.278
2015 SCImago Journal Rankings: 1.129
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorNg, IOLen_HK
dc.contributor.authorPoon, RTPen_HK
dc.contributor.authorLee, JMFen_HK
dc.contributor.authorFan, STen_HK
dc.contributor.authorNg, Men_HK
dc.contributor.authorTso, WKen_HK
dc.date.accessioned2010-09-06T09:46:15Z-
dc.date.available2010-09-06T09:46:15Z-
dc.date.issued2001en_HK
dc.identifier.citationAmerican Journal Of Clinical Pathology, 2001, v. 116 n. 6, p. 838-845en_HK
dc.identifier.issn0002-9173en_HK
dc.identifier.urihttp://hdl.handle.net/10722/88657-
dc.description.abstractAssessment of angiogenesis may yield important information for an effective antiangiogenic treatment for hepatocellular carcinoma (HCC) because HCC is characteristically hypervascular. We examined the relationship of microvessel density (MVD), vascular endothelial growth factor (VEGF), and VEGF receptors Flt-1 and Flk-1/KDR in 50 patients with HCC and in 3 hepatoma cell lines. VEGF messenger RNA (mRNA) was overexpressed in 26 tumors (52%), and the 3 VEGF isoforms (121, 165, and 189) were present in high frequencies. Flt-1 mRNA was overexpressed in 34 tumors (68%), with levels significantly increased in HCCs compared with the nontumorous livers. Tumor Flt-1 mRNA significantly correlated with tumor VEGF mRNA levels. Within the group of tumors 8.5 cm or less in diameter, tumors with intrahepatic metastasis in the form of tumor microsatellite formation had significantly higher VEGF mRNA levels. MVD assessed by immunohistochemical analysis with CD34 antibody was inversely related to tumor size. Angiogenesis as assessed by MVD and tumor VEGF expression seems to have a more important role in tumor growth and intrahepatic metastasis in smaller HCCs. The differential up-regulation of Flt-1 suggests that it may have an important role in angiogenesis in HCC.en_HK
dc.languageengen_HK
dc.publisherAmerican Society for Clinical Pathology. The Journal's web site is located at http://www.ajcp.comen_HK
dc.relation.ispartofAmerican Journal of Clinical Pathologyen_HK
dc.subjectFlk-1/KDRen_HK
dc.subjectFlt-1en_HK
dc.subjectHepatocellular carcinomaen_HK
dc.subjectMicrovessel densityen_HK
dc.subjectVascular endothelial growth factoren_HK
dc.subjectVEGFen_HK
dc.subject.meshAdulten_HK
dc.subject.meshAgeden_HK
dc.subject.meshCarcinoma, Hepatocellular - blood supply - pathology - surgeryen_HK
dc.subject.meshDNA Primersen_HK
dc.subject.meshDNA, Neoplasm - analysisen_HK
dc.subject.meshEndothelial Growth Factors - genetics - metabolismen_HK
dc.subject.meshExtracellular Matrix Proteins - genetics - metabolismen_HK
dc.subject.meshFemaleen_HK
dc.subject.meshHumansen_HK
dc.subject.meshImmunoenzyme Techniquesen_HK
dc.subject.meshLiver Neoplasms - blood supply - pathology - surgeryen_HK
dc.subject.meshLymphokines - genetics - metabolismen_HK
dc.subject.meshMaleen_HK
dc.subject.meshMicrocirculationen_HK
dc.subject.meshMiddle Ageden_HK
dc.subject.meshNeovascularization, Pathologic - metabolismen_HK
dc.subject.meshRNA, Messenger - metabolismen_HK
dc.subject.meshReceptor Protein-Tyrosine Kinases - genetics - metabolismen_HK
dc.subject.meshReceptors, Growth Factor - genetics - metabolismen_HK
dc.subject.meshReceptors, Vascular Endothelial Growth Factoren_HK
dc.subject.meshReverse Transcriptase Polymerase Chain Reactionen_HK
dc.subject.meshTumor Cells, Cultured - metabolism - pathologyen_HK
dc.subject.meshVascular Endothelial Growth Factor Aen_HK
dc.subject.meshVascular Endothelial Growth Factor Receptor-1en_HK
dc.subject.meshVascular Endothelial Growth Factorsen_HK
dc.titleMicrovessel density, vascular endothelial growth factor and its receptors Flt-1 and Flk-1/KDR in hepatocellular carcinomaen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0002-9173&volume=116&spage=838&epage=845&date=2001&atitle=Microvessel+density,+vascular+endothelial+growth+factor+and+its+receptors+Flt-1+and+Flk-1/KDR+in+hepatocellular+carcinomaen_HK
dc.identifier.emailNg, IOL: iolng@hkucc.hku.hken_HK
dc.identifier.emailPoon, RTP: poontp@hkucc.hku.hken_HK
dc.identifier.emailFan, ST: stfan@hku.hken_HK
dc.identifier.authorityNg, IOL=rp00335en_HK
dc.identifier.authorityPoon, RTP=rp00446en_HK
dc.identifier.authorityFan, ST=rp00355en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1309/FXNL-QTN1-94FH-AB3Aen_HK
dc.identifier.pmid11764072-
dc.identifier.scopuseid_2-s2.0-0035190559en_HK
dc.identifier.hkuros66023en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0035190559&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume116en_HK
dc.identifier.issue6en_HK
dc.identifier.spage838en_HK
dc.identifier.epage845en_HK
dc.identifier.isiWOS:000172451700008-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridNg, IOL=7102753722en_HK
dc.identifier.scopusauthoridPoon, RTP=7103097223en_HK
dc.identifier.scopusauthoridLee, JMF=36065603500en_HK
dc.identifier.scopusauthoridFan, ST=7402678224en_HK
dc.identifier.scopusauthoridNg, M=7202076310en_HK
dc.identifier.scopusauthoridTso, WK=7006905486en_HK

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