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Activation of PLAG1...
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Afshari, Maryam K.Gothenburg University,Göteborgs universitet,Institutionen för biomedicin, avdelningen för laboratoriemedicin,Sahlgrenska Cancer Center,Department of Laboratory Medicine
(författare)
Activation of PLAG1 and HMGA2 by gene fusions involving the transcriptional regulator gene NFIB
- Artikel/kapitelEngelska2020
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LIBRIS-ID:oai:gup.ub.gu.se/295462
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https://gup.ub.gu.se/publication/295462URI
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https://doi.org/10.1002/gcc.22885DOI
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The pleomorphic adenoma (PA), which is the most common salivary gland neoplasm, is a benign tumor characterized by recurrent chromosome rearrangements involving 8q12 and 12q14-15. We have previously shown that thePLAG1andHMGA2oncogenes are the targets of these rearrangements. Here, we have identified previously unrecognized subsets of PAs with ins(9;8)/t(8;9) (n = 5) and ins(9;12)/t(9;12) (n = 8) and breakpoints located in the vicinity of thePLAG1andHMGA2loci. RNA-sequencing and reverse transcriptase (RT)-PCR analyses of a case with an ins(9;8) revealed a novelNFIB-PLAG1fusion in whichNFIBexon 4 is linked toPLAG1exon 3. In contrast to the developmentally regulatedPLAG1gene,NFIBwas highly expressed in normal salivary gland, indicating thatPLAG1in this case, as in other variant fusions, is activated by promoter swapping. RT-PCR analysis of three PAs with t(9;12) revealed two tumors with chimeric transcripts consisting ofHMGA2exon 4 linked toNFIBexons 9 or 3 and one case with a fusion linkingHMGA2exon 3 toNFIBexon 9. TheNFIBfusion events resulted in potent activation ofPLAG1andHMGA2. Analysis of the chromatin landscape surroundingNFIBrevealed several super-enhancers in the 5 '- and 3 '-parts of theNFIBlocus and its flanking sequences. These findings indicate thatPLAG1andHMGA2, similar toMYBin adenoid cystic carcinoma, may be activated by enhancer-hijacking events, in which super-enhancers inNFIBare translocated upstream ofPLAG1or downstream ofHMGA2. Our results further emphasize the role ofNFIBas a fusion partner to multiple oncogenes in histopathologically different types of salivary gland tumors.
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Fehr, AndreGothenburg University,Göteborgs universitet,Institutionen för biomedicin, avdelningen för laboratoriemedicin,Sahlgrenska Cancer Center,Department of Laboratory Medicine(Swepub:gu)xfehra
(författare)
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Nevado, PalomaGothenburg University,Göteborgs universitet,Sahlgrenska Cancer Center,Institutionen för biomedicin, avdelningen för laboratoriemedicin,Department of Laboratory Medicine(Swepub:gu)xtejpa
(författare)
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Andersson, Mattias K,1979Gothenburg University,Göteborgs universitet,Institutionen för biomedicin, avdelningen för laboratoriemedicin,Sahlgrenska Cancer Center,Department of Laboratory Medicine(Swepub:gu)xamatx
(författare)
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Stenman, Göran,1953Gothenburg University,Göteborgs universitet,Institutionen för biomedicin, avdelningen för laboratoriemedicin,Sahlgrenska Cancer Center,Department of Laboratory Medicine(Swepub:gu)xsteng
(författare)
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Göteborgs universitetInstitutionen för biomedicin, avdelningen för laboratoriemedicin
(creator_code:org_t)
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Ingår i:Genes Chromosomes & Cancer: Wiley59:11, s. 652-6601045-22571098-2264
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