Matches in SemOpenAlex for { <https://semopenalex.org/work/W2010914889> ?p ?o ?g. }
- W2010914889 endingPage "1580" @default.
- W2010914889 startingPage "1574" @default.
- W2010914889 abstract "Epigenetic alterations in the 11p15.5 imprinted gene cluster are frequent in human cancers and are associated with disordered imprinting of insulin-like growth factor (IGF)2 and H19. Recently, an imprinted gene cluster at 14q32 has been defined and includes two closely linked but reciprocally imprinted genes, DLK1 and GTL2, that have similarities to IGF2 and H19, respectively. Both GTL2 and H19 are maternally expressed RNAs with no protein product and display paternal allele promoter region methylation, and DLK1 and IGF2 are both paternally expressed. To determine whether methylation alterations within the 14q32 imprinted domain occur in human tumorigenesis, we investigated the status of the GTL2 promoter differentially methylated region (DMR) in 20 neuroblastoma tumours, 20 phaeochromocytomas and, 40 Wilms' tumours. Hypermethylation of the GTL2 promoter DMR was detected in 25% of neuroblastomas, 10% of phaeochromocytoma and 2.5% of Wilms' tumours. Tumours with GTL2 promoter DMR hypermethylation also demonstrated hypermethylation at an upstream intergenic DMR thought to represent a germline imprinting control element. Analysis of neuroblastoma cell lines revealed that GTL2 DMR hypermethylation was associated with transcriptional repression of GTL2. These epigenetic findings are similar to those reported in Wilms' tumours in which H19 repression and DMR hypermethylation is associated with loss of imprinting (LOI, biallelic expression) of IGF2. However, a neuroblastoma cell line with hypermethylation of the GTL2 promoter and intergenic DMR did not show LOI of DLK1 and although treatment with a demethylating agent restored GTL2 expression and reduced DLK1 expression. As described for IGF2/H19, epigenetic changes at DLK1/GTL2 occur in human cancers. However, these changes are not associated with DLK1 LOI highlighting differences in the imprinting control mechanisms operating in the IGF2-H19 and DLK1-GTL2 domains. GTL2 promoter and intergenic DMR hypermethylation is associated with the loss of GTL2 expression and this may contribute to tumorigenesis in a subset of human cancers." @default.
- W2010914889 created "2016-06-24" @default.
- W2010914889 creator A5008751369 @default.
- W2010914889 creator A5016534184 @default.
- W2010914889 creator A5065438005 @default.
- W2010914889 creator A5070386542 @default.
- W2010914889 creator A5073770568 @default.
- W2010914889 creator A5086644518 @default.
- W2010914889 creator A5088627051 @default.
- W2010914889 creator A5089755666 @default.
- W2010914889 creator A5090532039 @default.
- W2010914889 date "2005-03-29" @default.
- W2010914889 modified "2023-10-06" @default.
- W2010914889 title "Epigenetic alteration at the DLK1-GTL2 imprinted domain in human neoplasia: analysis of neuroblastoma, phaeochromocytoma and Wilms' tumour" @default.
- W2010914889 cites W1522971018 @default.
- W2010914889 cites W1967983465 @default.
- W2010914889 cites W1968892142 @default.
- W2010914889 cites W1994465394 @default.
- W2010914889 cites W2005528118 @default.
- W2010914889 cites W2019689602 @default.
- W2010914889 cites W2020284225 @default.
- W2010914889 cites W2023346582 @default.
- W2010914889 cites W2037265798 @default.
- W2010914889 cites W2043905028 @default.
- W2010914889 cites W2046534900 @default.
- W2010914889 cites W2055129041 @default.
- W2010914889 cites W2059267677 @default.
- W2010914889 cites W2065583064 @default.
- W2010914889 cites W2074180520 @default.
- W2010914889 cites W2076368721 @default.
- W2010914889 cites W2094889529 @default.
- W2010914889 cites W2096758563 @default.
- W2010914889 cites W2104632504 @default.
- W2010914889 cites W2106495164 @default.
- W2010914889 cites W2116032027 @default.
- W2010914889 cites W2125231020 @default.
- W2010914889 cites W2127282587 @default.
- W2010914889 cites W2140583698 @default.
- W2010914889 cites W2141737525 @default.
- W2010914889 cites W2144029692 @default.
- W2010914889 cites W2152703613 @default.
- W2010914889 cites W2159115343 @default.
- W2010914889 cites W2160423822 @default.
- W2010914889 cites W2162859804 @default.
- W2010914889 cites W2164252048 @default.
- W2010914889 doi "https://doi.org/10.1038/sj.bjc.6602478" @default.
- W2010914889 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/2362015" @default.
- W2010914889 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/15798773" @default.
- W2010914889 hasPublicationYear "2005" @default.
- W2010914889 type Work @default.
- W2010914889 sameAs 2010914889 @default.
- W2010914889 citedByCount "124" @default.
- W2010914889 countsByYear W20109148892012 @default.
- W2010914889 countsByYear W20109148892013 @default.
- W2010914889 countsByYear W20109148892014 @default.
- W2010914889 countsByYear W20109148892015 @default.
- W2010914889 countsByYear W20109148892016 @default.
- W2010914889 countsByYear W20109148892017 @default.
- W2010914889 countsByYear W20109148892018 @default.
- W2010914889 countsByYear W20109148892019 @default.
- W2010914889 countsByYear W20109148892020 @default.
- W2010914889 countsByYear W20109148892021 @default.
- W2010914889 countsByYear W20109148892022 @default.
- W2010914889 countsByYear W20109148892023 @default.
- W2010914889 crossrefType "journal-article" @default.
- W2010914889 hasAuthorship W2010914889A5008751369 @default.
- W2010914889 hasAuthorship W2010914889A5016534184 @default.
- W2010914889 hasAuthorship W2010914889A5065438005 @default.
- W2010914889 hasAuthorship W2010914889A5070386542 @default.
- W2010914889 hasAuthorship W2010914889A5073770568 @default.
- W2010914889 hasAuthorship W2010914889A5086644518 @default.
- W2010914889 hasAuthorship W2010914889A5088627051 @default.
- W2010914889 hasAuthorship W2010914889A5089755666 @default.
- W2010914889 hasAuthorship W2010914889A5090532039 @default.
- W2010914889 hasBestOaLocation W20109148891 @default.
- W2010914889 hasConcept C104317684 @default.
- W2010914889 hasConcept C150194340 @default.
- W2010914889 hasConcept C153911025 @default.
- W2010914889 hasConcept C190727270 @default.
- W2010914889 hasConcept C201492766 @default.
- W2010914889 hasConcept C2775999222 @default.
- W2010914889 hasConcept C2776715637 @default.
- W2010914889 hasConcept C33288867 @default.
- W2010914889 hasConcept C41091548 @default.
- W2010914889 hasConcept C502942594 @default.
- W2010914889 hasConcept C54355233 @default.
- W2010914889 hasConcept C555283112 @default.
- W2010914889 hasConcept C81885089 @default.
- W2010914889 hasConcept C86803240 @default.
- W2010914889 hasConcept C94715292 @default.
- W2010914889 hasConceptScore W2010914889C104317684 @default.
- W2010914889 hasConceptScore W2010914889C150194340 @default.
- W2010914889 hasConceptScore W2010914889C153911025 @default.
- W2010914889 hasConceptScore W2010914889C190727270 @default.
- W2010914889 hasConceptScore W2010914889C201492766 @default.
- W2010914889 hasConceptScore W2010914889C2775999222 @default.
- W2010914889 hasConceptScore W2010914889C2776715637 @default.
- W2010914889 hasConceptScore W2010914889C33288867 @default.