What is it about?
Understanding the consequences of whole genome duplication (i.e., tetraploidization) on genome stability and the phenotype of cancer cells. We address two major questions: 1) what cellular mechanisms involved in controlling the stability of the genome are affected upon tetraploidization, and 2) what benefit does the cancer cell obtain from whole genome duplication. This study shows that replication stress is triggered by polyploidization, suggesting a novel role of replication stress during tumor progression.
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Why is it important?
This study sheds new light on understanding the causes of one of the major hallmarks of cancer, i.e., genomic instability. Replication stress is associated, not only with structural aberrations, but also with numerical chromosome alterations, i.e., aneuploidy.
Perspectives
This study provided the chance to expand the current knowledge regarding the process of tetraploidy, which it has been shown to be greatly present during tumorigenesis. Exploring the causes and consequences of tetraploidy might open new venues for translational genomics.
Jordi Camps
Institut d'Investigacions Biomèdiques August Pi i Sunyer
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This page is a summary of: Near-tetraploid cancer cells show chromosome instability triggered by replication stress and exhibit enhanced invasiveness, The FASEB Journal, July 2018, Federation of American Societies For Experimental Biology (FASEB),
DOI: 10.1096/fj.201700247rr.
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