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Article: Expression of vascular endothelial growth factor and its receptors in the anaplastic progression of astrocytoma, oligodendroglioma, and ependymoma

TitleExpression of vascular endothelial growth factor and its receptors in the anaplastic progression of astrocytoma, oligodendroglioma, and ependymoma
Authors
KeywordsAngiogenesis
Ependymoma
Flt-1
Glioma
KDR
Oligodendroglioma
VEGF
Issue Date1998
PublisherLippincott Williams & Wilkins. The Journal's web site is located at http://www.ajsp.com
Citation
American Journal Of Surgical Pathology, 1998, v. 22 n. 7, p. 816-826 How to Cite?
AbstractVascular endothelial growth factor (VEGF) is a hypoxia-inducible angiogenic factor, which is known to be upregulated in most cases of glioblastoma multiforme (GBM). The expression of VEGF and its receptors in ependymomas, oligodendrogliomas, and particularly the expression during anaplastic progression of these three types of gliomas has not been studied extensively. Fifty-six gliomas, consisting of 10 ependymomas, 12 oligodendrogliomas, 3 anaplastic oligodendrogliomas, 6 astrocytomas grade II, 5 anaplastic astrocytomas, and 20 gliobiasroma multiformes, were investigated for VEGF and receptor expression using in situ hybridization (ISH) and reverse transcription polymerase chain reaction (RT-PCR). Results showed that VEGF was moderately to strongly expressed in 8 of 10 ependymomas and in all anaplastic oligodendrogliomas and glioblastoma multiforme cases. These tumors displayed similar degrees of extensive necrosis and vascular proliferation, with VEGF expression consistently seen in tumor cells around necrotic areas. The VEGF expression, although present at a lower level, also was shown in 4 of 12 oligodendrogliomas, in 3 of 6 astrocytomas grade II, and in 2 of 5 anaplastic astrocytomas, with a regional rather than diffuse pattern of positive result. The findings from the in situ hybridization study correlated with the expression index, as determined by reverse transcription polymerase chain reaction. Expression of VEGF was correlated significantly with vascular proliferation (p < l0 -5) and necrosis (p < 10 -5), as well as with microvessel density (p = 0.002, r(s) = 0.41). The VEGF receptors, kinase domain region (KDR) and Fms-like-tyrosine kinase (Flt-1), also were upregulated in the tumor vasculature of glioblastoma multiforme, anaplastic oligodendrogliomas, and ependymomas with necrosis; whereas the astrocytomas grade II, anaplastic astrocytomas, and oligodendroglioma tumors tended to express a weak to nondetectable signal. Anaplastic progression in all three types of gliomas is heralded by the occurrence of small zones of VEGF- expressing cells and early vascular proliferation, followed by an accelerated phase of angiogenesis closely associated with VEGF induction around areas of necrosis and with the expression of VEGF receptors in the tumor vasculature.
Persistent Identifierhttp://hdl.handle.net/10722/88570
ISSN
2015 Impact Factor: 4.951
2015 SCImago Journal Rankings: 2.393
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorChan, ASYen_HK
dc.contributor.authorLeung, SYen_HK
dc.contributor.authorWong, MPen_HK
dc.contributor.authorYuen, STen_HK
dc.contributor.authorCheung, Nen_HK
dc.contributor.authorFan, YWen_HK
dc.contributor.authorChung, LPen_HK
dc.date.accessioned2010-09-06T09:45:05Z-
dc.date.available2010-09-06T09:45:05Z-
dc.date.issued1998en_HK
dc.identifier.citationAmerican Journal Of Surgical Pathology, 1998, v. 22 n. 7, p. 816-826en_HK
dc.identifier.issn0147-5185en_HK
dc.identifier.urihttp://hdl.handle.net/10722/88570-
dc.description.abstractVascular endothelial growth factor (VEGF) is a hypoxia-inducible angiogenic factor, which is known to be upregulated in most cases of glioblastoma multiforme (GBM). The expression of VEGF and its receptors in ependymomas, oligodendrogliomas, and particularly the expression during anaplastic progression of these three types of gliomas has not been studied extensively. Fifty-six gliomas, consisting of 10 ependymomas, 12 oligodendrogliomas, 3 anaplastic oligodendrogliomas, 6 astrocytomas grade II, 5 anaplastic astrocytomas, and 20 gliobiasroma multiformes, were investigated for VEGF and receptor expression using in situ hybridization (ISH) and reverse transcription polymerase chain reaction (RT-PCR). Results showed that VEGF was moderately to strongly expressed in 8 of 10 ependymomas and in all anaplastic oligodendrogliomas and glioblastoma multiforme cases. These tumors displayed similar degrees of extensive necrosis and vascular proliferation, with VEGF expression consistently seen in tumor cells around necrotic areas. The VEGF expression, although present at a lower level, also was shown in 4 of 12 oligodendrogliomas, in 3 of 6 astrocytomas grade II, and in 2 of 5 anaplastic astrocytomas, with a regional rather than diffuse pattern of positive result. The findings from the in situ hybridization study correlated with the expression index, as determined by reverse transcription polymerase chain reaction. Expression of VEGF was correlated significantly with vascular proliferation (p < l0 -5) and necrosis (p < 10 -5), as well as with microvessel density (p = 0.002, r(s) = 0.41). The VEGF receptors, kinase domain region (KDR) and Fms-like-tyrosine kinase (Flt-1), also were upregulated in the tumor vasculature of glioblastoma multiforme, anaplastic oligodendrogliomas, and ependymomas with necrosis; whereas the astrocytomas grade II, anaplastic astrocytomas, and oligodendroglioma tumors tended to express a weak to nondetectable signal. Anaplastic progression in all three types of gliomas is heralded by the occurrence of small zones of VEGF- expressing cells and early vascular proliferation, followed by an accelerated phase of angiogenesis closely associated with VEGF induction around areas of necrosis and with the expression of VEGF receptors in the tumor vasculature.en_HK
dc.languageengen_HK
dc.publisherLippincott Williams & Wilkins. The Journal's web site is located at http://www.ajsp.comen_HK
dc.relation.ispartofAmerican Journal of Surgical Pathologyen_HK
dc.rightsAmerican Journal of Surgical Pathology. Copyright © Lippincott Williams & Wilkins.en_HK
dc.subjectAngiogenesisen_HK
dc.subjectEpendymomaen_HK
dc.subjectFlt-1en_HK
dc.subjectGliomaen_HK
dc.subjectKDRen_HK
dc.subjectOligodendrogliomaen_HK
dc.subjectVEGFen_HK
dc.subject.meshAstrocytoma - blood supply - metabolism - pathologyen_HK
dc.subject.meshBrain Neoplasms - blood supply - metabolism - pathologyen_HK
dc.subject.meshDNA Primers - chemistryen_HK
dc.subject.meshDisease Progressionen_HK
dc.subject.meshEndothelial Growth Factors - genetics - metabolismen_HK
dc.subject.meshEpendymoma - blood supply - metabolism - pathologyen_HK
dc.subject.meshHumansen_HK
dc.subject.meshImmunoenzyme Techniquesen_HK
dc.subject.meshIn Situ Hybridizationen_HK
dc.subject.meshLymphokines - genetics - metabolismen_HK
dc.subject.meshNeovascularization, Pathologic - metabolismen_HK
dc.subject.meshOligodendroglioma - blood supply - metabolism - pathologyen_HK
dc.subject.meshPolymerase Chain Reactionen_HK
dc.subject.meshProto-Oncogene Proteins - metabolismen_HK
dc.subject.meshRNA, Messenger - metabolismen_HK
dc.subject.meshRNA, Neoplasm - metabolismen_HK
dc.subject.meshReceptor Protein-Tyrosine Kinases - metabolismen_HK
dc.subject.meshReceptors, Growth Factor - metabolismen_HK
dc.subject.meshReceptors, Vascular Endothelial Growth Factoren_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.titleExpression of vascular endothelial growth factor and its receptors in the anaplastic progression of astrocytoma, oligodendroglioma, and ependymomaen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0147-5185&volume=22&issue=7&spage=816&epage=826&date=1998&atitle=Expression+of+vascular+endothelial+growth+factor+and+its+receptors+in+the+anaplastic+progression+of+astrocytoma,+oligodendroglioma,+and+ependymomaen_HK
dc.identifier.emailLeung, SY: suetyi@hku.hken_HK
dc.identifier.emailWong, MP: mwpik@hkucc.hku.hken_HK
dc.identifier.emailChung, LP: lpchung@hkucc.hku.hken_HK
dc.identifier.authorityLeung, SY=rp00359en_HK
dc.identifier.authorityWong, MP=rp00348en_HK
dc.identifier.authorityChung, LP=rp00249en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1097/00000478-199807000-00004en_HK
dc.identifier.pmid9669344-
dc.identifier.scopuseid_2-s2.0-0031868650en_HK
dc.identifier.hkuros40703en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0031868650&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume22en_HK
dc.identifier.issue7en_HK
dc.identifier.spage816en_HK
dc.identifier.epage826en_HK
dc.identifier.isiWOS:000074610100004-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridChan, ASY=55246984000en_HK
dc.identifier.scopusauthoridLeung, SY=7202044886en_HK
dc.identifier.scopusauthoridWong, MP=7403907887en_HK
dc.identifier.scopusauthoridYuen, ST=7103160927en_HK
dc.identifier.scopusauthoridCheung, N=36803314200en_HK
dc.identifier.scopusauthoridFan, YW=7403492523en_HK
dc.identifier.scopusauthoridChung, LP=24315879100en_HK

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