pubmed-article:16160013 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:16160013 | lifeskim:mentions | umls-concept:C0006826 | lld:lifeskim |
pubmed-article:16160013 | lifeskim:mentions | umls-concept:C0441471 | lld:lifeskim |
pubmed-article:16160013 | lifeskim:mentions | umls-concept:C0040649 | lld:lifeskim |
pubmed-article:16160013 | lifeskim:mentions | umls-concept:C1426344 | lld:lifeskim |
pubmed-article:16160013 | lifeskim:mentions | umls-concept:C0332183 | lld:lifeskim |
pubmed-article:16160013 | pubmed:issue | 1 | lld:pubmed |
pubmed-article:16160013 | pubmed:dateCreated | 2005-12-23 | lld:pubmed |
pubmed-article:16160013 | pubmed:abstractText | The Polo-like kinases (Plks) are a highly conserved family of protein kinases that function in regulation of cell cycle and DNA damage-induced checkpoints. Evidence of a tumor suppressor function for the Plks in human neoplasia is lacking. Here, we report that Snk/Plk2 is transcriptionally down-regulated in B-cell neoplasms. Silencing occurs with very high frequency in Burkitt lymphoma (BL) but is also detected in B-cell neoplasms of other types and is associated with aberrant cytosine methylation in the CpG island located at the 5' end of the SNK/PLK2 gene. Silencing is specific to malignant B cells because SNK/PLK2 was unmethylated (and expressed) in primary B lymphocytes, in EBV-immortalized B lymphoblastoid cell lines (LCLs), and in adenocarcinomas (of the breast) and squamous-cell carcinomas (of the head and neck). Expression of Snk/Plk2 in BL cell lines was restored by demethylating agents. The related PLK1 and PLK3 (FNK/PRK) genes were overexpressed in BL cell lines lacking Snk/Plk2 expression, consistent with functional degeneracy among the Plk family. Ectopic expression of Snk/Plk2 in BL cells resulted in apoptosis, a potential mechanistic basis underlying the strong selective pressure for abrogation of Snk/Plk2 function in B-cell neoplasia. | lld:pubmed |
pubmed-article:16160013 | pubmed:language | eng | lld:pubmed |
pubmed-article:16160013 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:16160013 | pubmed:citationSubset | AIM | lld:pubmed |
pubmed-article:16160013 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:16160013 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:16160013 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:16160013 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:16160013 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:16160013 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:16160013 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:16160013 | pubmed:month | Jan | lld:pubmed |
pubmed-article:16160013 | pubmed:issn | 0006-4971 | lld:pubmed |
pubmed-article:16160013 | pubmed:author | pubmed-author:SullivanAlexa... | lld:pubmed |
pubmed-article:16160013 | pubmed:author | pubmed-author:FarrellPaul... | lld:pubmed |
pubmed-article:16160013 | pubmed:author | pubmed-author:CrookTimT | lld:pubmed |
pubmed-article:16160013 | pubmed:author | pubmed-author:SmithPaulP | lld:pubmed |
pubmed-article:16160013 | pubmed:author | pubmed-author:SpenderLindsa... | lld:pubmed |
pubmed-article:16160013 | pubmed:author | pubmed-author:HoffmannIngri... | lld:pubmed |
pubmed-article:16160013 | pubmed:author | pubmed-author:SyedNeloferN | lld:pubmed |
pubmed-article:16160013 | pubmed:author | pubmed-author:O'NionsJennyJ | lld:pubmed |
pubmed-article:16160013 | pubmed:author | pubmed-author:CrawfordDorot... | lld:pubmed |
pubmed-article:16160013 | pubmed:author | pubmed-author:DyerMartinM | lld:pubmed |
pubmed-article:16160013 | pubmed:author | pubmed-author:KarranLorrain... | lld:pubmed |
pubmed-article:16160013 | pubmed:author | pubmed-author:AlldayMartinM | lld:pubmed |
pubmed-article:16160013 | pubmed:author | pubmed-author:GriffinBeverl... | lld:pubmed |
pubmed-article:16160013 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:16160013 | pubmed:day | 1 | lld:pubmed |
pubmed-article:16160013 | pubmed:volume | 107 | lld:pubmed |
pubmed-article:16160013 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:16160013 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:16160013 | pubmed:pagination | 250-6 | lld:pubmed |
pubmed-article:16160013 | pubmed:dateRevised | 2011-11-2 | lld:pubmed |
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pubmed-article:16160013 | pubmed:meshHeading | pubmed-meshheading:16160013... | lld:pubmed |
pubmed-article:16160013 | pubmed:year | 2006 | lld:pubmed |
pubmed-article:16160013 | pubmed:articleTitle | Transcriptional silencing of Polo-like kinase 2 (SNK/PLK2) is a frequent event in B-cell malignancies. | lld:pubmed |
pubmed-article:16160013 | pubmed:affiliation | Breakthrough Breast Cancer Centre, Institute of Cancer Research, Fulham Rd, London SW3 6JB, United Kingdom. | lld:pubmed |
pubmed-article:16160013 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:16160013 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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