U.S. Department of Defense

 

Authors

Hendrik Witt, German Cancer Research Center
Stephen C. Mack, Hospital for Sick Children
Marina Ryzhova, NN Burdenko Neurosurgical Institute
Sebastian Bender, German Cancer Research Center
Martin Sill, German Cancer Research Center
Ruth Isserlin, University of Toronto
Axel Benner, German Cancer Research Center
Thomas Hielscher, German Cancer Research Center
Till Milde, University Hospital Heidelberg
Marc Remke, German Cancer Research Center
David T. W. Jones, German Cancer Research Center
Paul A. Northcott, Hospital for Sick Children
Livia Garzia, Hospital for Sick Children
Kelsey C. Bertrand, Hospital for Sick Children
Andrea Wittmann, German Cancer Research Center
Yuan Yao, Hospital for Sick Children, Toronto
Stephen S. Roberts, Uniformed Services University of the Health Sciences
Luca Massimi, Catholic University School of Medicine
Tim Van Meter, Virginia Commonwealth University
William A. Weiss, University of California - San Francisco
Nalin Gupta, University of California - San Francisco
Wiesia Grajkowska, University of Warsaw
Boleslaw Lach, McMaster University
Yoon-Jae Cho, Children’s Hospital Boston
Andreas von Deimling, University of Heidelberg
Andreas E. Kulozik, University Hospital Heidelberg
Olaf Witt, University Hospital Heidelberg
Gary D. Bader, University of Toronto
Cynthia E. Hawkins, Hospital for Sick Children
Uri Tabori, Hospital for Sick Children
Abhijit Guha, Hospital for Sick Children
James T. Rutka, Hospital for Sick Children
Peter Lichter, German Cancer Research Center
Andrey Korshunov, University of Heidelberg
Michael D. Taylor, Hospital for Sick ChildrenFollow
Stefan M. Pfister, German Cancer Research CenterFollow

Date of this Version

2011

Comments

Published in Cancer Cell (2011) 20, 143–157; DOI 10.1016/j.ccr.2011.07.007

Abstract

Despite the histological similarity of ependymomas from throughout the neuroaxis, the disease likely comprises multiple independent entities, each with a distinct molecular pathogenesis. Transcriptional profiling of two large independent cohorts of ependymoma reveals the existence of two demographically, transcriptionally, genetically, and clinically distinct groups of posterior fossa (PF) ependymomas. Group A patients are younger, have laterally located tumors with a balanced genome, and are much more likely to exhibit recurrence, metastasis at recurrence, and death compared with Group B patients. Identification and optimization of immunohistochemical (IHC) markers for PF ependymoma subgroups allowed validation of our findings on a third independent cohort, using a human ependymoma tissue microarray, and provides a tool for prospective prognostication and stratification of PF ependymoma patients.

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