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 Blood, 1 January 2006, Vol. 107, No. 1, pp. 250-256.
Prepublished online as a Blood First Edition Paper on September 13, 2005; DOI 10.1182/blood-2005-03-1194.

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NEOPLASIA

Transcriptional silencing of Polo-like kinase 2 (SNK/PLK2) is a frequent event in B-cell malignancies

Nelofer Syed, Paul Smith, Alexandra Sullivan, Lindsay C. Spender, Martin Dyer, Lorraine Karran, Jenny O'Nions, Martin Allday, Ingrid Hoffmann, Dorothy Crawford, Beverley Griffin, Paul J. Farrell, and Tim Crook

From the Breakthrough Breast Cancer Centre, Institute of Cancer Research, London, United Kingdom; Ludwig Institute for Cancer Research, University College London, London, United Kingdom; Beatson Institute for Cancer Research, Growth Factor Signalling Laboratory, Garscube Estate, Bearsden, Glasgow, United Kingdom; Medical Research Council Toxicology Unit, University of Leicester Medical School, Leicester, United Kingdom; Department of Virology, Imperial College Faculty of Medicine, St Mary's Campus, London, United Kingdom; Cell Cycle Control and Carcinogenesis, F045, German Cancer Research Center DKFZ, Heidelberg, Germany; Department of Veterinary Pathology, University of Edinburgh, Edinburgh, United Kingdom.

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.


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