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- W1976979641 abstract "Members of the nuclear factor-κB (NF-κB) family of transcriptional regulators are central mediators of the cellular inflammatory response. Although constitutive NF-κB signalling is present in most human tumours, mutations in pathway members are rare, complicating efforts to understand and block aberrant NF-κB activity in cancer. Here we show that more than two-thirds of supratentorial ependymomas contain oncogenic fusions between RELA, the principal effector of canonical NF-κB signalling, and an uncharacterized gene, C11orf95. In each case, C11orf95-RELA fusions resulted from chromothripsis involving chromosome 11q13.1. C11orf95-RELA fusion proteins translocated spontaneously to the nucleus to activate NF-κB target genes, and rapidly transformed neural stem cells--the cell of origin of ependymoma--to form these tumours in mice. Our data identify a highly recurrent genetic alteration of RELA in human cancer, and the C11orf95-RELA fusion protein as a potential therapeutic target in supratentorial ependymoma." @default.
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- W1976979641 date "2014-02-19" @default.
- W1976979641 modified "2023-10-12" @default.
- W1976979641 title "C11orf95–RELA fusions drive oncogenic NF-κB signalling in ependymoma" @default.
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- W1976979641 doi "https://doi.org/10.1038/nature13109" @default.
- W1976979641 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4050669" @default.
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