Illicit survival of cancer cells during polyploidization and depolyploidization

I. Vitale, L. Galluzzi, L. Senovilla, A. Criollo, M. Jemaá, M. Castedo, G. Kroemer

Research output: Contribution to journalArticlepeer-review


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.

Original languageEnglish
Pages (from-to)1403-1413
Number of pages11
JournalCell Death and Differentiation
Issue number9
Publication statusPublished - Sep 2011


  • aneuploidy
  • cancer
  • mitosis
  • tetraploid
  • TP53

ASJC Scopus subject areas

  • Cell Biology
  • Molecular Biology


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