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dc.date.accessioned2020-10-28T19:23:52Z
dc.date.available2020-10-28T19:23:52Z
dc.date.created2020-10-14T20:26:39Z
dc.date.issued2020
dc.identifier.citationSiaw, Joachim Tetteh Javanmardi, Niloufar Van den Eynden, Jimmy Lind, Dan Emil Fransson, Susanne Martinez-Monleon, Angela Djos, Anna Sjöberg, Rose-Marie Östensson, Malin Carén, Helena Trøen, Gunhild Beiske, Klaus Berbegall, Ana P. Noguera, Rosa Lai, Wei-Yun Kogner, Per Palmer, Ruth H. Hallberg, Bengt Martinsson, Tommy . 11q deletion or ALK activity curbs DLG2 expression to maintain an undifferentiated state in neuroblastoma. Cell reports. 2020, 32:108171(12), 1-24
dc.identifier.urihttp://hdl.handle.net/10852/80771
dc.description.abstractHigh-risk neuroblastomas typically display an undifferentiated or poorly differentiated morphology. It is therefore vital to understand molecular mechanisms that block the differentiation process. We identify an important role for oncogenic ALK-ERK1/2-SP1 signaling in the maintenance of undifferentiated neural crest-derived progenitors through the repression of DLG2, a candidate tumor suppressor gene in neuroblastoma. DLG2 is expressed in the murine “bridge signature” that represents the transcriptional transition state when neural crest cells or Schwann cell precursors differentiate to chromaffin cells of the adrenal gland. We show that the restoration of DLG2 expression spontaneously drives neuroblastoma cell differentiation, highlighting the importance of DLG2 in this process. These findings are supported by genetic analyses of high-risk 11q deletion neuroblastomas, which identified genetic lesions in the DLG2 gene. Our data also suggest that further exploration of other bridge genes may help elucidate the mechanisms underlying the differentiation of NC-derived progenitors and their contribution to neuroblastomas.
dc.languageEN
dc.publisherCell Press
dc.rightsAttribution 4.0 International
dc.rights.urihttps://creativecommons.org/licenses/by/4.0/
dc.title11q deletion or ALK activity curbs DLG2 expression to maintain an undifferentiated state in neuroblastoma
dc.typeJournal article
dc.creator.authorSiaw, Joachim Tetteh
dc.creator.authorJavanmardi, Niloufar
dc.creator.authorVan den Eynden, Jimmy
dc.creator.authorLind, Dan Emil
dc.creator.authorFransson, Susanne
dc.creator.authorMartinez-Monleon, Angela
dc.creator.authorDjos, Anna
dc.creator.authorSjöberg, Rose-Marie
dc.creator.authorÖstensson, Malin
dc.creator.authorCarén, Helena
dc.creator.authorTrøen, Gunhild
dc.creator.authorBeiske, Klaus
dc.creator.authorBerbegall, Ana P.
dc.creator.authorNoguera, Rosa
dc.creator.authorLai, Wei-Yun
dc.creator.authorKogner, Per
dc.creator.authorPalmer, Ruth H.
dc.creator.authorHallberg, Bengt
dc.creator.authorMartinsson, Tommy
cristin.unitcode185,53,18,13
cristin.unitnameAvdeling for patologi
cristin.ispublishedtrue
cristin.fulltextoriginal
cristin.qualitycode1
dc.identifier.cristin1839693
dc.identifier.bibliographiccitationinfo:ofi/fmt:kev:mtx:ctx&ctx_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.jtitle=Cell reports&rft.volume=32:108171&rft.spage=1&rft.date=2020
dc.identifier.jtitleCell reports
dc.identifier.volume32
dc.identifier.issue12
dc.identifier.doihttps://doi.org/10.1016/j.celrep.2020.108171
dc.identifier.urnURN:NBN:no-83857
dc.type.documentTidsskriftartikkel
dc.type.peerreviewedPeer reviewed
dc.source.issn2211-1247
dc.identifier.fulltextFulltext https://www.duo.uio.no/bitstream/handle/10852/80771/2/Postnr%2B1839693_Beiske_PAT.pdf
dc.type.versionPublishedVersion
cristin.articleid108171


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