| pubmed-article:18216295 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:18216295 | lifeskim:mentions | umls-concept:C0598766 | lld:lifeskim |
| pubmed-article:18216295 | lifeskim:mentions | umls-concept:C0596290 | lld:lifeskim |
| pubmed-article:18216295 | lifeskim:mentions | umls-concept:C0288331 | lld:lifeskim |
| pubmed-article:18216295 | lifeskim:mentions | umls-concept:C0020507 | lld:lifeskim |
| pubmed-article:18216295 | lifeskim:mentions | umls-concept:C0442805 | lld:lifeskim |
| pubmed-article:18216295 | lifeskim:mentions | umls-concept:C1332397 | lld:lifeskim |
| pubmed-article:18216295 | lifeskim:mentions | umls-concept:C0450407 | lld:lifeskim |
| pubmed-article:18216295 | lifeskim:mentions | umls-concept:C1517945 | lld:lifeskim |
| pubmed-article:18216295 | pubmed:issue | 7 | lld:pubmed |
| pubmed-article:18216295 | pubmed:dateCreated | 2008-3-25 | lld:pubmed |
| pubmed-article:18216295 | pubmed:abstractText | The kinase inhibitors imatinib mesylate and dasatinib are the preferred treatment for Philadelphia chromosome-positive (Ph+) leukemias, and they are highly successful in the chronic phase of chronic myeloid leukemia (CML). However, they are not efficient in Ph+ B-cell acute lymphoblastic leukemia (B-ALL). Ph+ leukemia cells are highly resistant to apoptosis, and evidence from cell lines and primary cells suggest Bcl-xL as a critical mediator of resistance to apoptosis: however, this concept has never been rigorously tested in an animal model. To clarify the role of Bcl-xL in Ph+ B-ALL, we generated 2 mouse models. In the first model, Ph+ B-ALL and loss of Bcl-xL expression are coinduced; in the second model, leukemia is induced with expression of Bcl-xL protein well above the levels found in wild-type lymphoblasts. Deletion of Bcl-xL did not inhibit leukemogenesis or affect apoptosis, but increased cellular proliferation. Consistent with this result, overexpression of Bcl-xL led to decreased cellular proliferation. These models reveal an unexpected role for Bcl-xL in cell-cycle entry and the proliferation of tumor cells. | lld:pubmed |
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| pubmed-article:18216295 | pubmed:language | eng | lld:pubmed |
| pubmed-article:18216295 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:18216295 | pubmed:citationSubset | AIM | lld:pubmed |
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| pubmed-article:18216295 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:18216295 | pubmed:month | Apr | lld:pubmed |
| pubmed-article:18216295 | pubmed:issn | 0006-4971 | lld:pubmed |
| pubmed-article:18216295 | pubmed:author | pubmed-author:HuettnerClaud... | lld:pubmed |
| pubmed-article:18216295 | pubmed:author | pubmed-author:HarbJason GJG | lld:pubmed |
| pubmed-article:18216295 | pubmed:author | pubmed-author:ChylaBrenda... | lld:pubmed |
| pubmed-article:18216295 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:18216295 | pubmed:day | 1 | lld:pubmed |
| pubmed-article:18216295 | pubmed:volume | 111 | lld:pubmed |
| pubmed-article:18216295 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:18216295 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:18216295 | pubmed:pagination | 3760-9 | lld:pubmed |
| pubmed-article:18216295 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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