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Article: Pilocytic astrocytomas do not show most of the genetic changes commonly seen in diffuse astrocytomas

TitlePilocytic astrocytomas do not show most of the genetic changes commonly seen in diffuse astrocytomas
Authors
KeywordsChemicals And Cas Registry Numbers
Issue Date2000
PublisherBlackwell Publishing Ltd. The Journal's web site is located at http://www.blackwellpublishing.com/journals/HIS
Citation
Histopathology, 2000, v. 37 n. 5, p. 437-444 How to Cite?
AbstractAims: While it is well known that pilocytic astrocytomas are clinically distinct from diffuse astrocytomas, few comprehensive studies have focused on their genetic differences. The aim of this study was to examine pilocytic astrocytomas for genetic alterations that are commonly seen in diffuse astrocytomas. Methods and results: By using molecular genetic and immunohistochemical techniques, we evaluated p16, p53, CDK4 and PTEN genes in 29 pilocytic astrocytomas. Mutation screening of p53 and PTEN was performed by single strand conformation polymorphism analysis followed by direct sequencing. Loss of heterozygosity (LOH) of p53, p16 and 10q23-25 loci was performed with microsatellite markers and genomic microsatellite instability (MSI) was also screened. Protein expression of p16, p53, CDK4 and PTEN was examined by immunohistochemistry. Five tumours were found to have single genetic alterations, which included a p53 mutation, a PTEN mutation, MSI at a single microsatellite marker of the p16 locus, and one single LOH at each p16 and 10q23 loci. Protein expressions of p16, CDK4 and PTEN were detected in 73%, 61% and 38% of tumours, respectively. Significantly and in sharp contrast to diffuse astrocytomas, no pilocytic astrocytoma in our series stained for p53 protein. Conclusion: Pilocytic astrocytomas have neither MSI phenotype nor recurrent alterations of the p53 and p 16 genes. However, altered expression of PTEN may be important in the genesis of pilocytic astrocytomas. We conclude that pilocytic astrocytomas are genetically distinct from diffuse astrocytomas. Lack of p53 mutation/immunostaining may serve as a diagnostic adjunct for differentiating pilocytic astrocytomas from diffuse astrocytomas in small neurosurgical biopsies.
Persistent Identifierhttp://hdl.handle.net/10722/91280
ISSN
2015 Impact Factor: 3.425
2015 SCImago Journal Rankings: 1.488
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorCheng, Yen_HK
dc.contributor.authorPang, JC-Sen_HK
dc.contributor.authorNg, H-Ken_HK
dc.contributor.authorDing, Men_HK
dc.contributor.authorZhang, S-Fen_HK
dc.contributor.authorZheng, Jen_HK
dc.contributor.authorLiu, D-Gen_HK
dc.contributor.authorPoon, W-Sen_HK
dc.date.accessioned2010-09-17T10:16:08Z-
dc.date.available2010-09-17T10:16:08Z-
dc.date.issued2000en_HK
dc.identifier.citationHistopathology, 2000, v. 37 n. 5, p. 437-444en_HK
dc.identifier.issn0309-0167en_HK
dc.identifier.urihttp://hdl.handle.net/10722/91280-
dc.description.abstractAims: While it is well known that pilocytic astrocytomas are clinically distinct from diffuse astrocytomas, few comprehensive studies have focused on their genetic differences. The aim of this study was to examine pilocytic astrocytomas for genetic alterations that are commonly seen in diffuse astrocytomas. Methods and results: By using molecular genetic and immunohistochemical techniques, we evaluated p16, p53, CDK4 and PTEN genes in 29 pilocytic astrocytomas. Mutation screening of p53 and PTEN was performed by single strand conformation polymorphism analysis followed by direct sequencing. Loss of heterozygosity (LOH) of p53, p16 and 10q23-25 loci was performed with microsatellite markers and genomic microsatellite instability (MSI) was also screened. Protein expression of p16, p53, CDK4 and PTEN was examined by immunohistochemistry. Five tumours were found to have single genetic alterations, which included a p53 mutation, a PTEN mutation, MSI at a single microsatellite marker of the p16 locus, and one single LOH at each p16 and 10q23 loci. Protein expressions of p16, CDK4 and PTEN were detected in 73%, 61% and 38% of tumours, respectively. Significantly and in sharp contrast to diffuse astrocytomas, no pilocytic astrocytoma in our series stained for p53 protein. Conclusion: Pilocytic astrocytomas have neither MSI phenotype nor recurrent alterations of the p53 and p 16 genes. However, altered expression of PTEN may be important in the genesis of pilocytic astrocytomas. We conclude that pilocytic astrocytomas are genetically distinct from diffuse astrocytomas. Lack of p53 mutation/immunostaining may serve as a diagnostic adjunct for differentiating pilocytic astrocytomas from diffuse astrocytomas in small neurosurgical biopsies.en_HK
dc.languageengen_HK
dc.publisherBlackwell Publishing Ltd. The Journal's web site is located at http://www.blackwellpublishing.com/journals/HISen_HK
dc.relation.ispartofHistopathologyen_HK
dc.subjectChemicals And Cas Registry Numbersen_HK
dc.titlePilocytic astrocytomas do not show most of the genetic changes commonly seen in diffuse astrocytomasen_HK
dc.typeArticleen_HK
dc.identifier.emailCheng, Y:yuecheng@hku.hken_HK
dc.identifier.authorityCheng, Y=rp1320en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1046/j.1365-2559.2000.01005.xen_HK
dc.identifier.pmid11119125-
dc.identifier.scopuseid_2-s2.0-0033731127en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0033731127&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume37en_HK
dc.identifier.issue5en_HK
dc.identifier.spage437en_HK
dc.identifier.epage444en_HK
dc.identifier.isiWOS:000165904200007-

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