| pubmed-article:15870198 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:15870198 | lifeskim:mentions | umls-concept:C0079427 | lld:lifeskim |
| pubmed-article:15870198 | lifeskim:mentions | umls-concept:C0039194 | lld:lifeskim |
| pubmed-article:15870198 | lifeskim:mentions | umls-concept:C0205282 | lld:lifeskim |
| pubmed-article:15870198 | lifeskim:mentions | umls-concept:C0214604 | lld:lifeskim |
| pubmed-article:15870198 | lifeskim:mentions | umls-concept:C1511681 | lld:lifeskim |
| pubmed-article:15870198 | lifeskim:mentions | umls-concept:C1707931 | lld:lifeskim |
| pubmed-article:15870198 | pubmed:issue | 19 | lld:pubmed |
| pubmed-article:15870198 | pubmed:dateCreated | 2005-5-11 | lld:pubmed |
| pubmed-article:15870198 | pubmed:abstractText | Expression of SHP-1 phosphatase, a key negative regulator of cell signaling, is lost in T cell lymphomas and other malignancies due to DNA methylation of the SHP-1 promoter by a currently undefined mechanism. We demonstrate that malignant T cells express DNA methyltransferase (DNMT) 1 and that constantly activated signal transducer and activator of transcription (STAT) 3 is capable of binding in vitro to DNA oligonucleotides corresponding to four STAT3 SIE/GAS binding sites identified in the SHP-1 promoter. STAT3, DNMT1, and histone deacetylase 1 form complexes and bind to the SHP-1 promoter in vivo. Treatment with pharmacologic grade DNMT1 anti-sense oligonucleotides and STAT3 small-interfering RNA induces in the malignant T cells DNA demethylation and expression of SHP-1 gene. These data indicate that STAT3 may, in part, transform cells by inducing epigenetic silencing of SHP-1 in cooperation with DNMT1 and, apparently, histone deacetylase 1. Reversal of such gene silencing represents an attractive aim for novel anticancer therapies. | lld:pubmed |
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| pubmed-article:15870198 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:15870198 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:15870198 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:15870198 | pubmed:month | May | lld:pubmed |
| pubmed-article:15870198 | pubmed:issn | 0027-8424 | lld:pubmed |
| pubmed-article:15870198 | pubmed:author | pubmed-author:ZhangQianQ | lld:pubmed |
| pubmed-article:15870198 | pubmed:author | pubmed-author:WasikMariusz... | lld:pubmed |
| pubmed-article:15870198 | pubmed:author | pubmed-author:WangHong YHY | lld:pubmed |
| pubmed-article:15870198 | pubmed:author | pubmed-author:RaghunathPuth... | lld:pubmed |
| pubmed-article:15870198 | pubmed:author | pubmed-author:NagasawaTomoh... | lld:pubmed |
| pubmed-article:15870198 | pubmed:author | pubmed-author:MarzecMichalM | lld:pubmed |
| pubmed-article:15870198 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:15870198 | pubmed:day | 10 | lld:pubmed |
| pubmed-article:15870198 | pubmed:volume | 102 | lld:pubmed |
| pubmed-article:15870198 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:15870198 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:15870198 | pubmed:pagination | 6948-53 | lld:pubmed |
| pubmed-article:15870198 | pubmed:dateRevised | 2009-11-19 | lld:pubmed |
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