title: Lack of p53 function promotes radiation-induced mitotic catastrophe in mouse embryonic fibroblast cells.
abstract: BACKGROUND
  We have demonstrated that in some human cancer cells both chronic mild heat and ionizing radiation exposures induce a transient block in S and G2 phases of the cell cycle. During this delay, cyclin B1 protein accumulates to supranormal levels, cyclin B1-dependent kinase is activated, and abrogation of the G2/M checkpoint control occurs resulting in mitotic catastrophe (MC).
  
  
  RESULTS
  Using syngenic mouse embryonic fibroblasts (MEF) with wild-type or mutant p53, we now show that, while both cell lines exhibit delays in S/G2 phase post-irradiation, the mutant p53 cells show elevated levels of cyclin B1 followed by MC, while the wild-type p53 cells present both a lower accumulation of cyclin B1 and a lower frequency of MC.
  
  
  CONCLUSIONS
  These results are in line with studies reporting the role of p53 as a post-transcriptional regulator of cyclin B1 protein and confirm that dysregulation of cyclin B1 promote radiation-induced MC. These findings might be exploited to design strategies to augment the yield of MC in tumor cells that are resistant to radiation-induced apoptosis.
authors.affiliation: Department of Pathology, University of Iowa, Iowa City, IA 52242, USA. fiorenza-ianzini@uiowa.edu
authors.forename: Fiorenza
authors.initials: F
authors.lastname: Ianzini
authors.forename: Alessandro
authors.initials: A
authors.lastname: Bertoldo
authors.forename: Elizabeth A
authors.initials: EA
authors.lastname: Kosmacek
authors.forename: Stacia L
authors.initials: SL
authors.lastname: Phillips
authors.forename: Michael A
authors.initials: MA
authors.lastname: Mackey