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Cytokinesis defects and cancer
Susanne M A Lens1,2, René H Medema3,4
1Oncode Institute, Utrecht, Netherlands. s.m.a.lens@umcutrecht.nl.
Nature Reviews. Cancer
|December 8, 2018
Summary
Cytokinesis failure, leading to whole-genome doubling, is a frequent event in human cancers. This process drives tumor evolution and genetic diversification, promoting cancer development.
Area of Science:
- Cell biology
- Cancer research
- Genetics
Background:
- Whole-genome duplication and centrosome amplification from cytokinesis failure can drive tumorigenesis in experimental models.
- The role of cytokinesis failure in human cancer development remains unclear.
Purpose of the Study:
- To review evidence linking whole-genome doubling events to human cancers.
- To discuss the contribution of cytokinesis defects to tumorigenesis.
- To explore the role of tetraploidy in cancer progression and genetic diversification.
Main Methods:
- Review of existing literature and evidence on cytokinesis failure, whole-genome doubling, and cancer.
- Analysis of the role of tetraploid cells as a transitional state in cancer evolution.
- Discussion of genetic diversification mechanisms facilitated by cytokinesis defects.
Main Results:
- Whole-genome doubling events are frequently observed in human cancers.
- Cytokinesis defects contribute significantly to tumorigenesis.
- Tetraploid cells generated by cytokinesis defects serve as a transient state towards aneuploidy in cancer.
Conclusions:
- Cytokinesis failure is an important driver of human cancer development.
- Defects in cell division facilitate genetic instability and tumor evolution.
- Cytokinesis defects represent a key pathway in tumor evolution.
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