%0 Journal Article
%A Chudasama, Priya
%A Mughal, Sadaf Shabbir
%A Sanders, Mathijs A
%A Hübschmann, Daniel
%A Chung, Inn
%A Deeg, Katharina
%A Wong, Siao-Han
%A Rabe, Sophie
%A Hlevnjak, Mario
%A Zapatka, Marc
%A Ernst, Aurélie
%A Kleinheinz, Kortine
%A Schlesner, Matthias
%A Sieverling, Lina
%A Klink, Barbara
%A Schröck, Evelin
%A Hoogenboezem, Remco M
%A Kasper, Bernd
%A Heilig, Christoph E
%A Egerer, Gerlinde
%A Wolf, Stephan
%A von Kalle, Christof
%A Eils, Roland
%A Stenzinger, Albrecht
%A Weichert, Wilko
%A Glimm, Hanno
%A Gröschel, Stefan
%A Kopp, Hans-Georg
%A Omlor, Georg
%A Lehner, Burkhard
%A Bauer, Sebastian
%A Schimmack, Simon
%A Ulrich, Alexis
%A Mechtersheimer, Gunhild
%A Rippe, Karsten
%A Brors, Benedikt
%A Hutter, Barbara
%A Renner, Marcus
%A Hohenberger, Peter
%A Scholl, Claudia
%A Fröhling, Stefan
%T Integrative genomic and transcriptomic analysis of leiomyosarcoma.
%J Nature Communications
%V 9
%N 1
%@ 2041-1723
%C London
%I Nature Publishing Group
%M DKFZ-2018-00072
%P 144
%D 2018
%X Leiomyosarcoma (LMS) is an aggressive mesenchymal malignancy with few therapeutic options. The mechanisms underlying LMS development, including clinically actionable genetic vulnerabilities, are largely unknown. Here we show, using whole-exome and transcriptome sequencing, that LMS tumors are characterized by substantial mutational heterogeneity, near-universal inactivation of TP53 and RB1, widespread DNA copy number alterations including chromothripsis, and frequent whole-genome duplication. Furthermore, we detect alternative telomere lengthening in 78
%F PUB:(DE-HGF)16
%9 Journal Article
%$ pmid:29321523
%2 pmc:PMC5762758
%R 10.1038/s41467-017-02602-0
%U https://inrepo02.dkfz.de/record/131775