Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2006-8-14
pubmed:abstractText
Centrosome abnormalities are observed in human cancers and have been associated with aneuploidy, a driving force in tumour progression. However, the exact pathways that tend to cause centrosome abnormalities have not been fully elucidated in human tumours. Using a series of 68 non-small-cell lung carcinomas and an array of in vitro experiments, the relationship between centrosome abnormalities, aneuploidy, and the status of key G1 to S-phase transition cell-cycle molecules, involved in the regulation of centrosome duplication, was investigated. Centrosome amplification and structural abnormalities were common (53%), were strongly related to aneuploidy, and, surprisingly, were even seen in adjacent hyperplastic regions, suggesting the possibility that these are early lesions in lung carcinogenesis. Cyclin E and E2F1 overexpression, but not p53 mutation, was observed to correlate with centrosome abnormalities in vivo (p = 0.029 and p = 0.015, respectively). This was further strengthened by the observation that cyclin E was specifically present in the nucleus and/or cytoplasm of the cells that contained centrosome aberrations. The cytoplasmic cyclin E signal may be attributed, in part, to the presence of truncated low-molecular-weight isoforms of cyclin E. In order to isolate the effect of cyclin E on the appearance of centrosome abnormalities, a U2OS tetracycline-repressible cyclin E cell line that has a normal centrosome profile by default was used. With this system, it was confirmed in vitro that persistent cyclin E overexpression is sufficient to cause the appearance of centrosome abnormalities.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0022-3417
pubmed:author
pubmed:copyrightInfo
Copyright 2006 Pathological Society of Great Britain and Ireland.
pubmed:issnType
Print
pubmed:volume
209
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
512-21
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:16739112-Aged, pubmed-meshheading:16739112-Aneuploidy, pubmed-meshheading:16739112-Carcinoma, Non-Small-Cell Lung, pubmed-meshheading:16739112-Centrosome, pubmed-meshheading:16739112-Chi-Square Distribution, pubmed-meshheading:16739112-Cyclin E, pubmed-meshheading:16739112-E2F1 Transcription Factor, pubmed-meshheading:16739112-Electrophoresis, Polyacrylamide Gel, pubmed-meshheading:16739112-Female, pubmed-meshheading:16739112-Gene Expression, pubmed-meshheading:16739112-Gene Expression Regulation, Neoplastic, pubmed-meshheading:16739112-Genes, p53, pubmed-meshheading:16739112-Humans, pubmed-meshheading:16739112-In Situ Hybridization, pubmed-meshheading:16739112-Lung Neoplasms, pubmed-meshheading:16739112-Male, pubmed-meshheading:16739112-Middle Aged, pubmed-meshheading:16739112-Statistics, Nonparametric
pubmed:year
2006
pubmed:articleTitle
Centrosome abnormalities are frequently observed in non-small-cell lung cancer and are associated with aneuploidy and cyclin E overexpression.
pubmed:affiliation
Molecular Carcinogenesis Group, Laboratory of Histology-Embryology, Medical School, University of Athens, Greece.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't