| pubmed-article:19287094 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:19287094 | lifeskim:mentions | umls-concept:C0023418 | lld:lifeskim |
| pubmed-article:19287094 | lifeskim:mentions | umls-concept:C1533585 | lld:lifeskim |
| pubmed-article:19287094 | lifeskim:mentions | umls-concept:C0038250 | lld:lifeskim |
| pubmed-article:19287094 | lifeskim:mentions | umls-concept:C0040690 | lld:lifeskim |
| pubmed-article:19287094 | lifeskim:mentions | umls-concept:C0531832 | lld:lifeskim |
| pubmed-article:19287094 | lifeskim:mentions | umls-concept:C1704259 | lld:lifeskim |
| pubmed-article:19287094 | lifeskim:mentions | umls-concept:C1705987 | lld:lifeskim |
| pubmed-article:19287094 | lifeskim:mentions | umls-concept:C1881379 | lld:lifeskim |
| pubmed-article:19287094 | pubmed:issue | 4 | lld:pubmed |
| pubmed-article:19287094 | pubmed:dateCreated | 2009-4-2 | lld:pubmed |
| pubmed-article:19287094 | pubmed:abstractText | Chromosome translocation to generate the TEL-AML1 (also known as ETV6-RUNX1) chimeric fusion gene is a frequent and early or initiating event in childhood acute lymphoblastic leukemia (ALL). Our starting hypothesis was that the TEL-AML1 protein generates and maintains preleukemic clones and that conversion to overt disease requires secondary genetic changes, possibly in the context of abnormal immune responses. Here, we show that a murine B cell progenitor cell line expressing inducible TEL-AML1 proliferates at a slower rate than parent cells but is more resistant to further inhibition of proliferation by TGF-beta. This facilitates the competitive expansion of TEL-AML1-expressing cells in the presence of TGF-beta. Further analysis indicated that TEL-AML1 binds to a principal TGF-beta signaling target, Smad3, and compromises its ability to activate target promoters. In mice expressing a TEL-AML1 transgene, early, pre-pro-B cells were increased in number and also showed reduced sensitivity to TGF-beta-mediated inhibition of proliferation. Moreover, expression of TEL-AML1 in human cord blood progenitor cells led to the expansion of a candidate preleukemic stem cell population that had an early B lineage phenotype (CD34+CD38-CD19+) and a marked growth advantage in the presence of TGF-beta. Collectively, these data suggest a plausible mechanism by which dysregulated immune responses to infection might promote the malignant evolution of TEL-AML1-expressing preleukemic clones. | lld:pubmed |
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| pubmed-article:19287094 | pubmed:language | eng | lld:pubmed |
| pubmed-article:19287094 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19287094 | pubmed:citationSubset | AIM | lld:pubmed |
| pubmed-article:19287094 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:19287094 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:19287094 | pubmed:month | Apr | lld:pubmed |
| pubmed-article:19287094 | pubmed:issn | 1558-8238 | lld:pubmed |
| pubmed-article:19287094 | pubmed:author | pubmed-author:GreavesMelM | lld:pubmed |
| pubmed-article:19287094 | pubmed:author | pubmed-author:CazzanigaGiov... | lld:pubmed |
| pubmed-article:19287094 | pubmed:author | pubmed-author:EnverTariqT | lld:pubmed |
| pubmed-article:19287094 | pubmed:author | pubmed-author:FordAnthony... | lld:pubmed |
| pubmed-article:19287094 | pubmed:author | pubmed-author:BuenoClaraC | lld:pubmed |
| pubmed-article:19287094 | pubmed:author | pubmed-author:KnightDeborah... | lld:pubmed |
| pubmed-article:19287094 | pubmed:author | pubmed-author:HongDengliD | lld:pubmed |
| pubmed-article:19287094 | pubmed:author | pubmed-author:PalmiChiaraC | lld:pubmed |
| pubmed-article:19287094 | pubmed:author | pubmed-author:CardusPennyP | lld:pubmed |
| pubmed-article:19287094 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:19287094 | pubmed:volume | 119 | lld:pubmed |
| pubmed-article:19287094 | pubmed:owner | NLM | lld:pubmed |
