2n or not 2n: Aneuploidy,polyploidy and chromosomal instability in primary and tumor cells |
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| Institution: | 1. Department of Cell and Regenerative Biology, University of Wisconsin, Madison, WI 53705, USA;2. Molecular and Cellular Pharmacology Training Program, University of Wisconsin, Madison, WI 53705, USA;3. Carbone Cancer Center, University of Wisconsin, Madison, WI 53705, USA;1. Institute of Pathology, University of Würzburg, Würzburg, Germany;2. Comprehensive Cancer Center Mainfranken, University Hospital Würzburg, Würzburg, Germany;1. Department of Molecular Biosciences, USA;2. Department of Nutritional Sciences, University of Texas at Austin, USA;1. Hubrecht Institute, Royal Netherlands Academy of Arts and Sciences (KNAW), Uppsalalaan 8, 3584 CT Utrecht, The Netherlands;2. Cancer Genomics Netherlands, University Medical Center Utrecht, 3584 CG, Utrecht, The Netherlands;3. Center for Molecular Medicine, University Medical Center Utrecht, 3584 CG, Utrecht, The Netherlands;1. Ludwig Institute for Cancer Research, USA;2. Department of Cellular & Molecular Medicine, University of California San Diego, La Jolla, CA 92093, USA;3. The Institute of Cancer Research, London, UK;1. Department of Mechanistic Cell Biology, Max Planck Institute of Molecular Physiology, Dortmund, Germany;2. Centre for Medical Biotechnology, Faculty of Biology, University Duisburg-Essen, Essen, Germany |
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| Abstract: | Mitotic defects leading to aneuploidy have been recognized as a hallmark of tumor cells for over 100 years. Current data indicate that ∼85% of human cancers have missegregated chromosomes to become aneuploid. Some maintain a stable aneuploid karyotype, while others consistently missegregate chromosomes over multiple divisions due to chromosomal instability (CIN). Both aneuploidy and CIN serve as markers of poor prognosis in diverse human cancers. Despite this, aneuploidy is generally incompatible with viability during development, and some aneuploid karyotypes cause a proliferative disadvantage in somatic cells. In vivo, the intentional introduction of aneuploidy can promote tumors, suppress them, or do neither. Here, we summarize current knowledge of the effects of aneuploidy and CIN on proliferation and cell death in nontransformed cells, as well as on tumor promotion, suppression, and prognosis. |
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