Linked Life Data

18666809

Source:http://linkedlifedata.com/resource/pubmed/id/18666809

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2008-7-31
pubmed:abstractText
The repair of ionizing radiation-induced potentially lethal damage (PLD) is suggested to be important for the clinical response to radiotherapy. PLD repair is usually studied in quiescent cultures prepared by growing cells to confluence with an accumulation of cells in G(0) phase of the cell cycle, but the biological pathways enabling PLD repair are still unknown. In this study, we examined whether the controlled expression of two different inducers of G(0) cell cycle arrest, the human tumor suppressor gene growth arrest specific 1 (GAS1) in murine fibroblasts and the forkhead transcription factor FOXO3a in human colon carcinoma cells, is sufficient to enable PLD repair. We found that GAS1 and FOXO3a induced a cell cycle arrest in G(0) phase with a concomitant reduction of proliferation of log-phase cells. In both cell systems, this cell cycle arrest in G(0) phase did not enable PLD repair in log-phase cells. Significant PLD repair was found in all confluent cultures that showed similar cell cycle distributions, while GAS1 and FOXO3a in confluent cells did not influence PLD repair. No differences were found in cell cycle re-entry after replating cells with different capacities for PLD repair. Our data suggest that the induction of G(0) cell cycle arrest and the reduction of proliferation are not sufficient to enable PLD repair.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0033-7587
pubmed:author
pubmed:issnType
Print
pubmed:volume
170
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
184-91
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed:year
2008
pubmed:articleTitle
G0 cell cycle arrest alone is insufficient for enabling the repair of ionizing radiation-induced potentially lethal damage.
pubmed:affiliation
Academic Medical Center, Laboratory for Experimental Oncology and Radiobiology, Department of Radiation Oncology, University of Amsterdam, Amsterdam, The Netherlands. c.vanbree@amc.uva.nl
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't