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Article: Subgroup-specific alternative splicing in medulloblastoma

TitleSubgroup-specific alternative splicing in medulloblastoma
Authors
KeywordsAlternative splicing
Medulloblastoma
Molecular subgroup
Neuronal development
Pediatric cancer
Issue Date2012
Citation
Acta Neuropathologica, 2012, v. 123, n. 4, p. 485-499 How to Cite?
AbstractMedulloblastoma comprises four distinct molecular variants: WNT, SHH, Group 3, and Group 4. We analyzed alternative splicing usage in 14 normal cerebellar samples and 103 medulloblastomas of known subgroup. Medulloblastoma samples have a statistically significant increase in alternative splicing as compared to normal fetal cerebella (2.3-times; P < 6.47E-8). Splicing patterns are distinct and specific between molecular subgroups. Unsupervised hierarchical clustering of alternative splicing events accurately assigns medulloblastomas to their correct subgroup. Subgroup-specific splicing and alternative promoter usage was most prevalent in Group 3 (19.4%) and SHH (16.2%) medulloblastomas, while observed less frequently in WNT (3.2%), and Group 4 (9.3%) tumors. Functional annotation of alternatively spliced genes reveals overrepresentation of genes important for neuronal development. Alternative splicing events in medulloblastoma may be regulated in part by the correlative expression of antisense transcripts, suggesting a possible mechanism affecting subgroup-specific alternative splicing. Our results identify additional candidate markers for medulloblastoma subgroup affiliation, further support the existence of distinct subgroups of the disease, and demonstrate an additional level of transcriptional heterogeneity between medulloblastoma subgroups. © Springer-Verlag 2012.
Persistent Identifierhttp://hdl.handle.net/10722/313989
ISSN
2023 Impact Factor: 9.3
2023 SCImago Journal Rankings: 4.720
PubMed Central ID
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorDubuc, Adrian M.-
dc.contributor.authorMorrissy, A. Sorana-
dc.contributor.authorKloosterhof, Nanne K.-
dc.contributor.authorNorthcott, Paul A.-
dc.contributor.authorYu, Emily P.Y.-
dc.contributor.authorShih, David-
dc.contributor.authorPeacock, John-
dc.contributor.authorGrajkowska, Wieslawa-
dc.contributor.authorVan Meter, Timothy-
dc.contributor.authorEberhart, Charles G.-
dc.contributor.authorPfister, Stefan-
dc.contributor.authorMarra, Marco A.-
dc.contributor.authorWeiss, William A.-
dc.contributor.authorScherer, Stephen W.-
dc.contributor.authorRutka, James T.-
dc.contributor.authorFrench, Pim J.-
dc.contributor.authorTaylor, Michael D.-
dc.date.accessioned2022-07-06T11:28:44Z-
dc.date.available2022-07-06T11:28:44Z-
dc.date.issued2012-
dc.identifier.citationActa Neuropathologica, 2012, v. 123, n. 4, p. 485-499-
dc.identifier.issn0001-6322-
dc.identifier.urihttp://hdl.handle.net/10722/313989-
dc.description.abstractMedulloblastoma comprises four distinct molecular variants: WNT, SHH, Group 3, and Group 4. We analyzed alternative splicing usage in 14 normal cerebellar samples and 103 medulloblastomas of known subgroup. Medulloblastoma samples have a statistically significant increase in alternative splicing as compared to normal fetal cerebella (2.3-times; P < 6.47E-8). Splicing patterns are distinct and specific between molecular subgroups. Unsupervised hierarchical clustering of alternative splicing events accurately assigns medulloblastomas to their correct subgroup. Subgroup-specific splicing and alternative promoter usage was most prevalent in Group 3 (19.4%) and SHH (16.2%) medulloblastomas, while observed less frequently in WNT (3.2%), and Group 4 (9.3%) tumors. Functional annotation of alternatively spliced genes reveals overrepresentation of genes important for neuronal development. Alternative splicing events in medulloblastoma may be regulated in part by the correlative expression of antisense transcripts, suggesting a possible mechanism affecting subgroup-specific alternative splicing. Our results identify additional candidate markers for medulloblastoma subgroup affiliation, further support the existence of distinct subgroups of the disease, and demonstrate an additional level of transcriptional heterogeneity between medulloblastoma subgroups. © Springer-Verlag 2012.-
dc.languageeng-
dc.relation.ispartofActa Neuropathologica-
dc.subjectAlternative splicing-
dc.subjectMedulloblastoma-
dc.subjectMolecular subgroup-
dc.subjectNeuronal development-
dc.subjectPediatric cancer-
dc.titleSubgroup-specific alternative splicing in medulloblastoma-
dc.typeArticle-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1007/s00401-012-0959-7-
dc.identifier.pmid22358458-
dc.identifier.pmcidPMC3984840-
dc.identifier.scopuseid_2-s2.0-84862688169-
dc.identifier.volume123-
dc.identifier.issue4-
dc.identifier.spage485-
dc.identifier.epage499-
dc.identifier.eissn1432-0533-
dc.identifier.isiWOS:000301849000004-

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