TY  - JOUR
AU  - Chudasama, Priya
AU  - Mughal, Sadaf Shabbir
AU  - Sanders, Mathijs A
AU  - Hübschmann, Daniel
AU  - Chung, Inn
AU  - Deeg, Katharina
AU  - Wong, Siao-Han
AU  - Rabe, Sophie
AU  - Hlevnjak, Mario
AU  - Zapatka, Marc
AU  - Ernst, Aurélie
AU  - Kleinheinz, Kortine
AU  - Schlesner, Matthias
AU  - Sieverling, Lina
AU  - Klink, Barbara
AU  - Schröck, Evelin
AU  - Hoogenboezem, Remco M
AU  - Kasper, Bernd
AU  - Heilig, Christoph E
AU  - Egerer, Gerlinde
AU  - Wolf, Stephan
AU  - von Kalle, Christof
AU  - Eils, Roland
AU  - Stenzinger, Albrecht
AU  - Weichert, Wilko
AU  - Glimm, Hanno
AU  - Gröschel, Stefan
AU  - Kopp, Hans-Georg
AU  - Omlor, Georg
AU  - Lehner, Burkhard
AU  - Bauer, Sebastian
AU  - Schimmack, Simon
AU  - Ulrich, Alexis
AU  - Mechtersheimer, Gunhild
AU  - Rippe, Karsten
AU  - Brors, Benedikt
AU  - Hutter, Barbara
AU  - Renner, Marcus
AU  - Hohenberger, Peter
AU  - Scholl, Claudia
AU  - Fröhling, Stefan
TI  - Integrative genomic and transcriptomic analysis of leiomyosarcoma.
JO  - Nature Communications
VL  - 9
IS  - 1
SN  - 2041-1723
CY  - London
PB  - Nature Publishing Group
M1  - DKFZ-2018-00072
SP  - 144
PY  - 2018
AB  - 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
LB  - PUB:(DE-HGF)16
C6  - pmid:29321523
C2  - pmc:PMC5762758
DO  - DOI:10.1038/s41467-017-02602-0
UR  - https://inrepo02.dkfz.de/record/131775
ER  -