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- Konrad H. Stopsack
- Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, NY 10065;
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- Charles A. Whittaker
- David H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, MA 02139;
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- Travis A. Gerke
- Department of Epidemiology, Harvard T. H. Chan School of Public Health, Boston, MA 02115;
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- Massimo Loda
- Department of Oncologic Pathology, Dana-Farber Cancer Institute, Boston, MA 02215;
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- Philip W. Kantoff
- Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, NY 10065;
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- Lorelei A. Mucci
- Department of Epidemiology, Harvard T. H. Chan School of Public Health, Boston, MA 02115;
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- Angelika Amon
- David H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, MA 02139;
抄録
<jats:title>Significance</jats:title> <jats:p>Aneuploidy is usually quantified by measuring intracellular DNA content or chromosome structure and number. We show that the number of altered chromosome arms can be estimated from transcriptome profiling, which allows for assessing aneuploidy within repositories of archival, formalin-fixed, paraffin-embedded tumors. While aneuploidy impedes proliferation in primary cells, we show that it is a feature of aggressiveness in primary prostate cancers that are more likely to become lethal. Our data suggest that losses or gains of entire chromosome arms confers aggressiveness beyond affecting copy numbers of tumor suppressors or oncogenes on those arms. Beyond helping understand the etiology of aggressive prostate cancer, we propose that extent of aneuploidy could also be employed clinically to inform risk stratification and treatment.</jats:p>
収録刊行物
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- Proceedings of the National Academy of Sciences
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Proceedings of the National Academy of Sciences 116 (23), 11390-11395, 2019-05-13
Proceedings of the National Academy of Sciences