Illicit survival of cancer cells during polyploidization and depolyploidization Review uri icon


MeSH Major

  • Neoplasms
  • Tetraploidy


  • Tetraploidy and the depolyploidization of tetraploid cells may contribute to oncogenesis. Several mechanisms have evolved to avoid the generation, survival, proliferation and depolyploidization of tetraploids. Cells that illicitly survive these checkpoints are prone to chromosomal instability and aneuploidization. Along with their replication, tetraploids constantly undergo chromosomal rearrangements that eventually lead to pseudodiploidy by two non-exclusive mechanisms: (i) multipolar divisions and (ii) illicit bipolar divisions in the presence of improper microtubule-kinetochore attachments. Here, we describe the regulation and the molecular mechanisms that underlie such a 'polyploidization-depolyploidization' cascade, while focusing on the role of oncogenes and tumor suppressor genes in tetraploidy-driven tumorigenesis. We speculate that the identification of signaling/metabolic cascades that are required for the survival of tetraploid or aneuploid (but not diploid) cancer cells may pave the way for the development of novel broad-spectrum anticancer agents.

publication date

  • September 2011



  • Review



  • eng

PubMed Central ID

  • PMC3178421

Digital Object Identifier (DOI)

  • 10.1038/cdd.2010.145

PubMed ID

  • 21072053

Additional Document Info

start page

  • 1403

end page

  • 13


  • 18


  • 9