Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
1987-4-15
pubmed:abstractText
It is proposed that tumor cell instability and the expression of cellular diversification mechanisms ensure that malignant neoplasms contain heterogeneous, phenotypically diverse tumor cell subpopulations. In such potentially unstable cellular mixtures of tumor cell phenotypes, some malignant cells may ultimately evolve with the most favorable properties for their progression to metastatic cells. Rates of cellular phenotypic instability and phenotypic diversification as well as their underlying causes appear to vary greatly among different tumor cells, and they are probably modulated by further genetic and chromosome changes and more frequently by intra- and extracellular epigenetic events that also differ, depending on the nature of the tumor cells and their cellular and microenvironmental interactions. Diversified malignant cells are characterized by quantitative and perhaps a few qualitative differences in gene expression, which may explain their abilities to undergo rapid changes in phenotypic properties. As tumor diversification and selection proceed uniquely in vivo, highly malignant cell subpopulations may eventually become dominant and gradually and independently lose their cellular and microenvironmental responsiveness. Tumor cell diversification mechanisms may be similar or identical to normal developmentally regulated diversification mechanisms that are used during embryonic and postembryonic cell diversification and development.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0008-5472
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
47
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1473-87
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed:year
1987
pubmed:articleTitle
Tumor cell instability, diversification, and progression to the metastatic phenotype: from oncogene to oncofetal expression.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Review, Research Support, Non-U.S. Gov't