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Labreche, Karim; Simeonova, Iva; Kamoun, Aurélie; Gleize, Vincent; Chubb, Daniel; Letouzé, Eric; Riazalhosseini, Yasser; Dobbins, Sara E.; Elarouci, Nabila; Ducray, Francois; de Reyniès, Aurélien; Zelenika, Diana; Wardell, Christopher P.; Frampton, Mathew; Saulnier, Olivier; Pastinen, Tomi; Hallout, Sabrina; Figarella-Branger, Dominique; Dehais, Caroline; Idbaih, Ahmed; Mokhtari, Karima; Delattre, Jean-Yves; Huillard, Emmanuelle; Mark Lathrop, G.; [...]

TCF12 is mutated in anaplastic oligodendroglioma

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  • Medientyp: E-Artikel
  • Titel: TCF12 is mutated in anaplastic oligodendroglioma
  • Beteiligte: Labreche, Karim; Simeonova, Iva; Kamoun, Aurélie; Gleize, Vincent; Chubb, Daniel; Letouzé, Eric; Riazalhosseini, Yasser; Dobbins, Sara E.; Elarouci, Nabila; Ducray, Francois; de Reyniès, Aurélien; Zelenika, Diana; Wardell, Christopher P.; Frampton, Mathew; Saulnier, Olivier; Pastinen, Tomi; Hallout, Sabrina; Figarella-Branger, Dominique; Dehais, Caroline; Idbaih, Ahmed; Mokhtari, Karima; Delattre, Jean-Yves; Huillard, Emmanuelle; Mark Lathrop, G.; [...]
  • Erschienen: Springer Science and Business Media LLC, 2015
  • Erschienen in: Nature Communications
  • Sprache: Englisch
  • DOI: 10.1038/ncomms8207
  • ISSN: 2041-1723
  • Entstehung:
  • Anmerkungen:
  • Beschreibung: <jats:title>Abstract</jats:title><jats:p>Anaplastic oligodendroglioma (AO) are rare primary brain tumours that are generally incurable, with heterogeneous prognosis and few treatment targets identified. Most oligodendrogliomas have chromosomes 1p/19q co-deletion and an <jats:italic>IDH</jats:italic> mutation. Here we analysed 51 AO by whole-exome sequencing, identifying previously reported frequent somatic mutations in <jats:italic>CIC</jats:italic> and <jats:italic>FUBP1</jats:italic>. We also identified recurrent mutations in <jats:italic>TCF12</jats:italic> and in an additional series of 83 AO. Overall, 7.5% of AO are mutated for <jats:italic>TCF12</jats:italic>, which encodes an oligodendrocyte-related transcription factor. Eighty percent of <jats:italic>TCF12</jats:italic> mutations identified were in either the bHLH domain, which is important for TCF12 function as a transcription factor, or were frameshift mutations leading to TCF12 truncated for this domain. We show that these mutations compromise <jats:italic>TCF12</jats:italic> transcriptional activity and are associated with a more aggressive tumour type. Our analysis provides further insights into the unique and shared pathways driving AO.</jats:p>
  • Zugangsstatus: Freier Zugang