Ontology type: schema:ScholarlyArticle Open Access: True
2014-11
AUTHORSWilliam Lee, Sewit Teckie, Thomas Wiesner, Leili Ran, Carlos N Prieto Granada, Mingyan Lin, Sinan Zhu, Zhen Cao, Yupu Liang, Andrea Sboner, William D Tap, Jonathan A Fletcher, Kety H Huberman, Li-Xuan Qin, Agnes Viale, Samuel Singer, Deyou Zheng, Michael F Berger, Yu Chen, Cristina R Antonescu, Ping Chi
ABSTRACTMalignant peripheral nerve sheath tumors (MPNSTs) represent a group of highly aggressive soft-tissue sarcomas that may occur sporadically, in association with neurofibromatosis type I (NF1 associated) or after radiotherapy. Using comprehensive genomic approaches, we identified loss-of-function somatic alterations of the Polycomb repressive complex 2 (PRC2) components (EED or SUZ12) in 92% of sporadic, 70% of NF1-associated and 90% of radiotherapy-associated MPNSTs. MPNSTs with PRC2 loss showed complete loss of trimethylation at lysine 27 of histone H3 (H3K27me3) and aberrant transcriptional activation of multiple PRC2-repressed homeobox master regulators and their regulated developmental pathways. Introduction of the lost PRC2 component in a PRC2-deficient MPNST cell line restored H3K27me3 levels and decreased cell growth. Additionally, we identified frequent somatic alterations of CDKN2A (81% of all MPNSTs) and NF1 (72% of non-NF1-associated MPNSTs), both of which significantly co-occur with PRC2 alterations. The highly recurrent and specific inactivation of PRC2 components, NF1 and CDKN2A highlights their critical and potentially cooperative roles in MPNST pathogenesis. More... »
PAGES1227-1232
http://scigraph.springernature.com/pub.10.1038/ng.3095
DOIhttp://dx.doi.org/10.1038/ng.3095
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PUBMEDhttps://www.ncbi.nlm.nih.gov/pubmed/25240281
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