Role of prolonged mitotic checkpoint activation in the formation and treatment of cancer

W. Brian Dalton, Vincent W. Yang

Research output: Contribution to journalReview articlepeer-review

Abstract

Mitotic abnormalities are a common feature of human cancer cells, and recent studies have provided evidence that such abnormalities may play a causative, rather than merely incidental role, in tumorigenesis. One such abnormality is prolonged activation of the mitotic checkpoint, which can be provoked by a number of the gene changes that drive tumor formation. At the same time, antimitotic chemotherapeutics exert their clinical efficacy through the largescale induction of prolonged mitotic checkpoint activation, indicating that mitotic arrest is influential in both the formation and treatment of human cancer. However, how this influence occurs is not well understood. In this perspective, we will discuss the current evidence in support of the potential mechanisms by which prolonged activation of the mitotic checkpoint affects both tumorigenesis and antimitotic chemotherapy.

Original languageEnglish (US)
Pages (from-to)1363-1370
Number of pages8
JournalFuture Oncology
Volume5
Issue number9
DOIs
StatePublished - 2009
Externally publishedYes

Keywords

  • Aneuploidy
  • Antimitotic chemotherapy
  • Apoptosis
  • Cell-cycle arrest
  • Centrosomes
  • Checkpoint
  • Chromosomal instability
  • DNA damage
  • Mitosis
  • Polypoidy
  • Tumorigenesis

ASJC Scopus subject areas

  • Oncology
  • Cancer Research

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