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Article: Genetic alterations in pediatric high-grade astrocytomas

TitleGenetic alterations in pediatric high-grade astrocytomas
Authors
KeywordsChemicals And Cas Registry Numbers
Issue Date1999
PublisherWB Saunders Co. The Journal's web site is located at http://www.elsevier.com/locate/humpath
Citation
Human Pathology, 1999, v. 30 n. 11, p. 1284-1290 How to Cite?
AbstractHigh-grade astrocytomas are tumors that are uncommon in children. Relatively few studies have been performed on their molecular properties and so it is not certain whether they follow different genetic pathways from those described in adult diffuse astrocytomas. In this study, we evaluated 24 pediatric high-grade astrocytomas (11 anaplastic astrocytomas and 13 glioblastomas) all of which were sporadic and primary. We studied mutations of p53, phosphatase and tensin homolog (PTEN), loss of heterozygosity (LOH) of chromosomes 17p13, 9p21 and 10q23-25, amplification of epidermal growth factor receptor (EGFR), and overexpression of EGFR and p53 protein. In addition, we searched for microsatellite instability (MSI) by using MSI sensitive and specific microsatellite markers, p53 mutations were found in 38% (9/24) of the high-grade astrocytomas and all brain stem tumors except 2 (71%, 5/7) had p53 mutations. PTEN mutations were found in 8% (2/24) of high- grade astrocytomas. However, no EGFR amplification was found in any of them. LOH was found at 17p13.1 in 50% (3/6 informative tumors), 9p21 in 83% (5/6 informative tumors), and 10q23-25 in 78% (7/9 informative tumors). Four tumors showed MSI, and 2 of them that showed widespread MSI were regarded as tumors with replication error (PER+) phenotype. All 4 tumors with MSI showed concurrent LOH of 9p21 and 10q23-25. Combining gene alterations, LOH, MSI, and gene mutations, inactivation of both alleles of PTEN and p53 was found in 57% (4/7 informative tumors) and 50% (3/6 informative tumors) of the cases respectively. We conclude that development of pediatric high-grade astrocytomas may follow pathways different from the primary or secondary paradigm of adult glioblastomas. In a subset of these tumors, genomic instability was also implicated.
Persistent Identifierhttp://hdl.handle.net/10722/91269
ISSN
2015 Impact Factor: 2.791
2015 SCImago Journal Rankings: 1.363
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorCheng, Yen_HK
dc.contributor.authorNg, H-Ken_HK
dc.contributor.authorZhang, S-Fen_HK
dc.contributor.authorDing, Men_HK
dc.contributor.authorPang, JC-Sen_HK
dc.contributor.authorZheng, Jen_HK
dc.contributor.authorPoon, W-Sen_HK
dc.date.accessioned2010-09-17T10:15:57Z-
dc.date.available2010-09-17T10:15:57Z-
dc.date.issued1999en_HK
dc.identifier.citationHuman Pathology, 1999, v. 30 n. 11, p. 1284-1290en_HK
dc.identifier.issn0046-8177en_HK
dc.identifier.urihttp://hdl.handle.net/10722/91269-
dc.description.abstractHigh-grade astrocytomas are tumors that are uncommon in children. Relatively few studies have been performed on their molecular properties and so it is not certain whether they follow different genetic pathways from those described in adult diffuse astrocytomas. In this study, we evaluated 24 pediatric high-grade astrocytomas (11 anaplastic astrocytomas and 13 glioblastomas) all of which were sporadic and primary. We studied mutations of p53, phosphatase and tensin homolog (PTEN), loss of heterozygosity (LOH) of chromosomes 17p13, 9p21 and 10q23-25, amplification of epidermal growth factor receptor (EGFR), and overexpression of EGFR and p53 protein. In addition, we searched for microsatellite instability (MSI) by using MSI sensitive and specific microsatellite markers, p53 mutations were found in 38% (9/24) of the high-grade astrocytomas and all brain stem tumors except 2 (71%, 5/7) had p53 mutations. PTEN mutations were found in 8% (2/24) of high- grade astrocytomas. However, no EGFR amplification was found in any of them. LOH was found at 17p13.1 in 50% (3/6 informative tumors), 9p21 in 83% (5/6 informative tumors), and 10q23-25 in 78% (7/9 informative tumors). Four tumors showed MSI, and 2 of them that showed widespread MSI were regarded as tumors with replication error (PER+) phenotype. All 4 tumors with MSI showed concurrent LOH of 9p21 and 10q23-25. Combining gene alterations, LOH, MSI, and gene mutations, inactivation of both alleles of PTEN and p53 was found in 57% (4/7 informative tumors) and 50% (3/6 informative tumors) of the cases respectively. We conclude that development of pediatric high-grade astrocytomas may follow pathways different from the primary or secondary paradigm of adult glioblastomas. In a subset of these tumors, genomic instability was also implicated.en_HK
dc.languageengen_HK
dc.publisherWB Saunders Co. The Journal's web site is located at http://www.elsevier.com/locate/humpathen_HK
dc.relation.ispartofHuman Pathologyen_HK
dc.subjectChemicals And Cas Registry Numbersen_HK
dc.titleGenetic alterations in pediatric high-grade 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.doi10.1016/S0046-8177(99)90057-6en_HK
dc.identifier.pmid10571506-
dc.identifier.scopuseid_2-s2.0-0032745828en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0032745828&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume30en_HK
dc.identifier.issue11en_HK
dc.identifier.spage1284en_HK
dc.identifier.epage1290en_HK
dc.identifier.isiWOS:000083596900003-

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