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dc.contributor.authorWarr, Tracy
dc.contributor.authorWard, Samantha
dc.contributor.authorBurrows, J.
dc.contributor.authorHarding, Brian
dc.contributor.authorWilkins, Peter
dc.contributor.authorHarkness, William
dc.contributor.authorHayward, Richard
dc.contributor.authorDarling, John L.
dc.contributor.authorThomas, David G.
dc.date.accessioned2008-01-23T14:48:17Z
dc.date.available2008-01-23T14:48:17Z
dc.date.issued2001
dc.identifier.citationGenes, Chromosomes and Cancer, 31(1): 15-22
dc.identifier.issn1045-2257
dc.identifier.pmid11284031
dc.identifier.doi10.1002/gcc.1113
dc.identifier.urihttp://hdl.handle.net/2436/16694
dc.descriptionMetadata only
dc.description.abstractAlthough astrocytomas are the most common central nervous system tumours in all age groups, there is substantial evidence that tumours arising in young patients (< 25 years of age) do not have the same genetic abnormalities that are characteristic of tumours in older patients. Furthermore, novel, consistent changes have not been identified in astrocytomas in children and young adults. We analysed 13 malignant astrocytomas from young patients using comparative genomic hybridisation. Regions of genomic imbalance were identified in 10 cases. The most common recurrent copy number aberrations were loss of 16p (54% of cases), 17p (38%), 19p (38%), and 22 (38%) and gain on 2q (38%), 12q (38%), 13 (38%), 4q (31%), 5q (31%), and 8q (31%). Seven regions of high copy number amplification were observed at 8q21-22 (three cases), 7q22-23 (two cases), and 1p21-22, 2q22, 12q13-pter, 12q15-21, and 13q11-14 (one case each). This study provides evidence of new characteristic chromosomal imbalances from which potential candidate genes involved in the development of malignant astrocytoma in children and young adults may be identified.
dc.language.isoen
dc.publisherWiley Interscience
dc.relation.urlhttp://www3.interscience.wiley.com/cgi-bin/abstract/77005859/
dc.subjectYoung adults
dc.subject.meshAdolescent
dc.subject.meshAdult
dc.subject.meshAstrocytoma
dc.subject.meshCentral Nervous System Neoplasms
dc.subject.meshChildren
dc.subject.meshChild, Preschool
dc.subject.meshChromosomal Aberrations
dc.subject.meshChromosome Disorders
dc.subject.meshFemale
dc.subject.meshGene Amplification
dc.subject.meshGene Dosage
dc.subject.meshHumans
dc.subject.meshIn Situ Hybridization
dc.subject.meshMale
dc.subject.meshSequence Deletion
dc.titleIdentification of extensive genomic loss and gain by comparative genomic hybridisation in malignant astrocytoma in children and young adults.
dc.typeJournal article
html.description.abstractAlthough astrocytomas are the most common central nervous system tumours in all age groups, there is substantial evidence that tumours arising in young patients (< 25 years of age) do not have the same genetic abnormalities that are characteristic of tumours in older patients. Furthermore, novel, consistent changes have not been identified in astrocytomas in children and young adults. We analysed 13 malignant astrocytomas from young patients using comparative genomic hybridisation. Regions of genomic imbalance were identified in 10 cases. The most common recurrent copy number aberrations were loss of 16p (54% of cases), 17p (38%), 19p (38%), and 22 (38%) and gain on 2q (38%), 12q (38%), 13 (38%), 4q (31%), 5q (31%), and 8q (31%). Seven regions of high copy number amplification were observed at 8q21-22 (three cases), 7q22-23 (two cases), and 1p21-22, 2q22, 12q13-pter, 12q15-21, and 13q11-14 (one case each). This study provides evidence of new characteristic chromosomal imbalances from which potential candidate genes involved in the development of malignant astrocytoma in children and young adults may be identified.


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