Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
18 Suppl
pubmed:dateCreated
1991-10-4
pubmed:abstractText
A group of coordinated cellular processes, not just one gene product, is responsible for invasion and metastasis, the most life-threatening aspect of cancer. It is now recognized that negative factors may be just as important as positive elements. Genetic changes causing an imbalance of growth regulation lead to uncontrolled proliferation necessary for both primary tumor and metastasis expansion. However, unrestrained growth does not, by itself, cause invasion and metastasis. This phenotype may require additional genetic changes. Thus, tumorigenicity and metastatic potential have both overlapping and separate features. Invasion and metastasis can be facilitated by proteins which stimulate tumor cell attachment to host cellular or extracellular matrix determinants, tumor cell proteolysis of host barriers, such as the basement membrane, tumor cell locomotion, and tumor cell colony formation in the target organ for metastasis. Facilitory proteins may act at many levels both intracellularly or extracellularly but are counterbalanced by factors which can block their production, regulation, or action. A common theme has emerged. In addition to loss of growth control, an imbalanced regulation of motility and proteolysis appears to be required for invasion and metastasis.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0008-5472
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
51
pubmed:geneSymbol
2 E1 a, A-raf, H-2Kb, H-ras, c-Ha-ras, c-fos, ras, v-fes, v-fms, v-ras, v-rat, v-src
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
5054s-5059s
pubmed:dateRevised
2005-11-16
pubmed:meshHeading
pubmed:year
1991
pubmed:articleTitle
Tumor invasion and metastasis: an imbalance of positive and negative regulation.
pubmed:affiliation
Laboratory of Pathology, National Cancer Institute, NIH, Bethesda, Maryland 20892.
pubmed:publicationType
Journal Article, Review