Linked Life Data

12539762

Source:http://linkedlifedata.com/resource/pubmed/id/12539762

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2003-1-22
pubmed:abstractText
When applied to the Colorado Plateau miner population, the two-stage clonal expansion (TSCE) model of radiation carcinogenesis predicts that radiation-induced promotion dominates radiation-induced initiation. Thus, according to the model, at least for alpha-particle radiation from inhaled radon daughters, lung cancer induction over long periods of protracted irradiation appears to be dominated by radiation-induced modification of the proliferation kinetics of already-initiated cells rather than by direct radiation-induced initiation (i.e., mutation) of normal cells. We explore the possible consequences of this result for radiation exposures to space travelers on long missions. Still unknown is the LET dependence of this effect. Speculations of the cause of this phenomenon include the suggestion that modification of cell kinetics is caused by a "bystander" effect, i.e., the traversal of normal cells by alpha particles, followed by the signaling of these cells to nearby initiated cells which then modify their proliferation kinetics.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
S
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0273-1177
pubmed:author
pubmed:copyrightInfo
c2002 COSPAR. Published by Elsevier Science Ltd. All rights reserved.
pubmed:issnType
Print
pubmed:volume
30
pubmed:owner
NASA
pubmed:authorsComplete
Y
pubmed:pagination
937-44
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
2002
pubmed:articleTitle
A new perspective of carcinogenesis from protracted high-LET radiation arises from the two-stage clonal expansion model.
pubmed:affiliation
Fred Hutchinson Cancer Research Center, Seattle, WA 98109-1024, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.