Checkpoint bypass and cell viability

Jon H. Chung, Yonggang Zhang, Fred Bunz

Research output: Contribution to journalArticle

Abstract

DNA damage impairs cell growth by delaying or preventing critical processes such as DNA replication and chromosome segregation. In normal proliferating cells, initiation of these processes is controlled by genetically-defined pathways known as checkpoints. Tumors often acquire mutations that disable checkpoints and cancer cells can therefore progress unimpeded into S-phase, through G2 and into mitosis with chromosomal DNA damage. Checkpoint bypass in cancer cells is associated with cell death and loss of proliferative capacity and therefore is believed to contribute to the efficacy of DNA-damaging therapies. Are cancer cell clones that bypass checkpoints invariably more sensitive to DNA damage than checkpoint-proficient cells in normal tissues? We present evidence that the inherent survival of damaged human cells can be surprisingly independent of checkpoint control.

Original languageEnglish (US)
Pages (from-to)2102-2107
Number of pages6
JournalCell cycle (Georgetown, Tex.)
Volume9
Issue number11
DOIs
StatePublished - Jun 1 2010

Fingerprint

Cell Survival
DNA Damage
Neoplasms
Chromosome Segregation
DNA Replication
S Phase
Mitosis
Genetic Therapy
Cell Death
Clone Cells
Mutation
Survival
Growth

Keywords

  • Cdk2
  • Checkpoint
  • Ionizing radiation
  • Mitosis
  • p53

ASJC Scopus subject areas

  • Cell Biology
  • Molecular Biology
  • Developmental Biology

Cite this

Checkpoint bypass and cell viability. / Chung, Jon H.; Zhang, Yonggang; Bunz, Fred.

In: Cell cycle (Georgetown, Tex.), Vol. 9, No. 11, 01.06.2010, p. 2102-2107.

Research output: Contribution to journalArticle

Chung, Jon H. ; Zhang, Yonggang ; Bunz, Fred. / Checkpoint bypass and cell viability. In: Cell cycle (Georgetown, Tex.). 2010 ; Vol. 9, No. 11. pp. 2102-2107.
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