Karyotypic Aberrations in Oncogenesis and Cancer Therapy Review uri icon


MeSH Major

  • Autophagy
  • Neoplasms
  • Tumor Suppressor Protein p53


  • © 2015 Elsevier Ltd.The propagation of whole-chromosome (aneuploid) or whole-genome (polyploid) defects is normally prevented by robust cell-intrinsic mechanisms. Moreover, non-diploid cells are under strict immunological surveillance. Nonetheless, tumors contain a high percentage of non-diploid genomes, indicating that malignant cells acquire the ability to bypass these control mechanisms and obtain a survival/proliferation benefit from bulky karyotypic defects. The non-diploid state imposes a significant metabolic burden on cancer cells and hence can be selectively targeted for therapeutic purposes. Here we discuss the impact of abnormal karyotypes on oncogenesis, tumor progression, and response to treatment, focusing on the biochemical and metabolic liabilities of non-diploid cells that can be harnessed for the development of novel chemo(immuno)therapeutic regimens against cancer.

publication date

  • October 2015



  • Review



  • eng

Digital Object Identifier (DOI)

  • 10.1016/j.trecan.2015.08.001

PubMed ID

  • 28741522

Additional Document Info

start page

  • 124

end page

  • 135


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