Linked Life Data

9920427

Source:http://linkedlifedata.com/resource/pubmed/id/9920427

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1999-2-5
pubmed:abstractText
Ultraviolet (UV) radiation contributes to the aetiology of melanoma, but the precise mechanistic details are still unclear. The CDKN2A gene which is associated with familial and sporadic melanoma, encodes a tumour suppressor, p16. We have previously shown that in response to low doses of UV radiation the level of p16 increases, and that this correlates with a G2 delay. Here we report that in melanoma cell lines which do not express p16, or express a mutant p16, no G2 delay is observed in response to UV. The loss of functional p16 also correlates with an increase in DNA damage as judged by increased numbers of bi- and multinuclear cells and cells containing 1-2 micronuclei following UV irradiation. This work provides a further link between UV radiation, CDKN2A and melanoma, suggesting that the functional inactivation of CDKN2A disrupts a p16-dependent G2 cell cycle checkpoint, thus contributing to the development of this neoplasm.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
0027-5107
pubmed:author
pubmed:issnType
Print
pubmed:day
9
pubmed:volume
422
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
43-53
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1998
pubmed:articleTitle
Involvement of p16CDKN2A in cell cycle delays after low dose UV irradiation.
pubmed:affiliation
Queensland Cancer Fund Cancer Unit, Queensland Institute of Medical Research, P.O. Royal Brisbane Hospital, Herston, Australia.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't