Linked Life Data

16868416

Source:http://linkedlifedata.com/resource/pubmed/id/16868416

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
12
pubmed:dateCreated
2006-7-25
pubmed:abstractText
The Polo-Like kinases (Plk) are a family of highly conserved cell cycle kinases, of which there are four members in humans. Whilst many studies support an oncogenic role for Plk1 in neoplasia, there is little definitive evidence at present to support involvement of the other family members in human cancer. Both Plk2 and Plk3 function in pathways of DNA damage response. Plk2 is a target gene for p53 and imposes a G2 checkpoint. More recent evidence reveals a novel function for Plk2 in mediating apoptosis in high grade B lymphomas. Epigenetic inactivation of Plk2 via aberrant CpG methylation in the transcriptional regulatory elements of the gene is a common event in B cell neoplasia, whereas epigenetic inactivation of Plk3 is exceedingly rare in lymphomas. Further, in every case lacking Plk2 expression, there is concomitant overexpression of Plk3, consistent with functional degeneracy between the two proteins. These results imply that Plk2 may function as a tumor suppressor in hematologic neoplasia and have pharmaco-epigenomic implications.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
1551-4005
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
5
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1262-4
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed:year
2006
pubmed:articleTitle
Epigenetic inactivation implies a tumor suppressor function in hematologic malignancies for Polo-like kinase 2 but not Polo-like kinase 3.
pubmed:affiliation
Cancer Genetics and Epigenetics Laboratory, The Toby Robins Breakthrough Breast Cancer Centre, Institute for Cancer Research, London, England.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't