Linked Life Data

19181515

Source:http://linkedlifedata.com/resource/pubmed/id/19181515

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2009-3-3
pubmed:abstractText
The phenomenon of replicative senescence was first observed more than 40 years ago by Hayflick who noted the inability of cultured human fibroblasts to proliferate indefinitely. The recent discovery that cellular senescence is triggered by many different activated oncogenes has led to the notion that senescence, like oncogene-induced apoptosis, serves as a critical and cell-autonomous tumor preventive mechanism. Both the DNA damage response and the ARF tumor suppressor have been mechanistically implicated in oncogene-induced senescence and the relative contributions of, and potential interactions between, these two pathways remain subjects of a lively debate. More recently, the discovery that cellular senescence can be bypassed during the epithelial-mesenchymal transition (EMT) that typically accompanies tumor progression, the observation that organ fibrosis is controlled by cellular senescence and, most noticeably, the mounting evidence linking cellular senescence to inflammation, make cellular senescence a still flaming hot subject after all these years.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
1879-0380
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
19
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
25-31
pubmed:meshHeading
pubmed:year
2009
pubmed:articleTitle
Cellular senescence: hot or what?
pubmed:affiliation
Department of Pathology and Helen Diller Family Comprehensive Cancer Center, University of California, San Francisco, CA 94143-0502, USA.
pubmed:publicationType
Journal Article, Review, Research Support, Non-U.S. Gov't