Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
11
pubmed:dateCreated
1994-10-20
pubmed:abstractText
Prolonged interferon (IFN) treatment can convert Moloney sarcoma-transformed mouse Balb C fibroblasts to a stable non-malignant status. The cells recover a number of differentiated features, which are maintained even when IFN is permanently omitted from the tissue culture medium. We show here that reversion could be at least in part attributed to constitutive IFN beta synthesized only in the reverted cells. The continued replication of these cells, although unable to induce tumours in athymic mice, could be the result of the maintained expression of an IFN antagonist termed sarcolectin (SCL), a balance being struck between the effects of v-mos oncogene, interferon beta and SCLs. In agreement with Lampl et al. [11], we suggest that normal cell growth is discontinuous, consisting of sudden bursts followed by prolonged arrests which could be necessary to promote differentiation during the ensuing interphase.
pubmed:language
fre
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
0764-4469
pubmed:author
pubmed:issnType
Print
pubmed:volume
316
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1286-9
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1993
pubmed:articleTitle
[Mechanism of proliferation of cells transformed by the Moloney mouse sarcoma virus after stable reversion to a non-malignant state].
pubmed:affiliation
Université Pierre-et-Marie-Curie, Laboratoire de Physiologie Cellulaire, Paris, France.
pubmed:publicationType
Journal Article, English Abstract