Linked Life Data

9806600

Source:http://linkedlifedata.com/resource/pubmed/id/9806600

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
1998-11-19
pubmed:abstractText
Cells from an infinite-life-span near-diploid human fibroblast cell strain, MSU-1.1, were transformed after a single exposure to 60Co gamma radiation. The frequency of transformation as measured by the number of induced foci per 10(6) cells was a linear function of dose. Cells from 13 independent foci from gamma-irradiated cell populations and one from a nonirradiated cell population were isolated, clonally expanded and assayed for characteristics of malignantly transformed cells. Eight of the 13 focus-derived cell strains from the irradiated populations formed tumors in athymic mice with latent periods (time required for the tumors to reach 1 cm in diameter) of 4-27 weeks. Of these 8 cell strains, 3 were fully growth factor-independent, formed large colonies (> 120 microm in diameter) in 0.33% agarose at a high frequency (50%), and produced malignant tumors with a mean latency of 6 weeks or less at all sites injected. Four others formed colonies in agarose at a slightly lower frequency, were only partially growth factor-independent, and produced malignant tumors with a longer mean latency (7-18 weeks). The tumor-derived cell lines from these latter 4 cell strains, when tested for growth in agarose, showed markedly enhanced anchorage independence. The eighth tumorigenic focus-derived cell strain was growth factor-independent but could not produce large colonies in agarose. It produced benign tumors (fibromas) with a mean latency of 27 weeks. All 8 tumorigenic focus-derived cell strains had lost the transactivating function of the TP53 (formerly known as p53) gene. However, loss of TP53 activity was not sufficient to cause tumorigenicity since 3 of the 6 nontumorigenic focus-derived cell strains had also lost all TP53 transactivation function. The other 3, which included a cell strain from the unirradiated control, had wild-type TP53 alleles and did not form tumors. These latter results support the hypothesis that loss of TP53 transactivating function plays a role in focus formation, but does not directly cause tumorigenicity. This is in agreement with studies that demonstrate that the loss of TP53 transactivation facilitates the other changes required for tumorigenicity.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
0033-7587
pubmed:author
pubmed:issnType
Print
pubmed:volume
150
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
577-84
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed:year
1998
pubmed:articleTitle
Dose-dependent transformation of cells of human fibroblast cell strain MSU-1.1 by cobalt-60 gamma radiation and characterization of the transformed cells.
pubmed:affiliation
Department of Biochemistry, The Cancer Center, Michigan State University, East Lansing 48824-1302, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, U.S. Gov't, Non-P.H.S., Research Support, Non-U.S. Gov't