pubmed-article:21689085 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:21689085 | lifeskim:mentions | umls-concept:C0086418 | lld:lifeskim |
pubmed-article:21689085 | lifeskim:mentions | umls-concept:C0007634 | lld:lifeskim |
pubmed-article:21689085 | lifeskim:mentions | umls-concept:C0023467 | lld:lifeskim |
pubmed-article:21689085 | lifeskim:mentions | umls-concept:C0026882 | lld:lifeskim |
pubmed-article:21689085 | lifeskim:mentions | umls-concept:C0287186 | lld:lifeskim |
pubmed-article:21689085 | lifeskim:mentions | umls-concept:C1332710 | lld:lifeskim |
pubmed-article:21689085 | lifeskim:mentions | umls-concept:C0237677 | lld:lifeskim |
pubmed-article:21689085 | lifeskim:mentions | umls-concept:C1268567 | lld:lifeskim |
pubmed-article:21689085 | pubmed:issue | 4 | lld:pubmed |
pubmed-article:21689085 | pubmed:dateCreated | 2011-7-28 | lld:pubmed |
pubmed-article:21689085 | pubmed:abstractText | The efficacy of tyrosine kinase (TK) inhibitors on non-cycling acute myeloid leukaemia (AML) cells, previously shown to have potent tumourigenic potential, is unknown. This pilot study describes the first attempt to characterize non-cycling cells from a small series of human FMS-like tyrosine kinase 3 (FLT3) mutation positive samples. CD34+ AML cells from patients with FLT3 mutation positive AML were cultured on murine stroma. In expansion cultures, non-cycling cells were found to retain CD34+ expression in contrast to dividing cells. Leukaemic gene rearrangements could be detected in non-cycling cells, indicating their leukaemic origin. Significantly, the FLT3-internal tandem duplication (ITD) mutation was found in the non-cycling fraction of four out of five cases. Exposure to the FLT3-directed inhibitor TKI258 clearly inhibited the growth of AML CD34+ cells in short-term cultures and colony-forming unit assays. Crucially, non-cycling cells were not eradicated, with the exception of one case, which exhibited exquisite sensitivity to the compound. Moreover, in longer-term cultures, TKI258-treated non-cycling cells showed no growth impairment compared to treatment-naive non-cycling cells. These findings suggest that non-cycling cells in AML may constitute a disease reservoir that is resistant to TK inhibition. Further studies with a larger sample size and other inhibitors are warranted. | lld:pubmed |
pubmed-article:21689085 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:21689085 | pubmed:language | eng | lld:pubmed |
pubmed-article:21689085 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:21689085 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:21689085 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:21689085 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:21689085 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:21689085 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:21689085 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:21689085 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:21689085 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:21689085 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:21689085 | pubmed:month | Aug | lld:pubmed |
pubmed-article:21689085 | pubmed:issn | 1365-2141 | lld:pubmed |
pubmed-article:21689085 | pubmed:author | pubmed-author:RoelLL | lld:pubmed |
pubmed-article:21689085 | pubmed:author | pubmed-author:MorganGarethG | lld:pubmed |
pubmed-article:21689085 | pubmed:author | pubmed-author:GreavesMelM | lld:pubmed |
pubmed-article:21689085 | pubmed:author | pubmed-author:TitleyIanI | lld:pubmed |
pubmed-article:21689085 | pubmed:author | pubmed-author:GonzalezDavid... | lld:pubmed |
pubmed-article:21689085 | pubmed:author | pubmed-author:BartolovicKer... | lld:pubmed |
pubmed-article:21689085 | pubmed:author | pubmed-author:YeungJennyJ | lld:pubmed |
pubmed-article:21689085 | pubmed:author | pubmed-author:AlvaresCaroli... | lld:pubmed |
pubmed-article:21689085 | pubmed:author | pubmed-author:SchenkTinoT | lld:pubmed |
pubmed-article:21689085 | pubmed:author | pubmed-author:Vijayaraghava... | lld:pubmed |
pubmed-article:21689085 | pubmed:author | pubmed-author:HulkkiSannaS | lld:pubmed |
pubmed-article:21689085 | pubmed:author | pubmed-author:SoChi W ECW | lld:pubmed |
pubmed-article:21689085 | pubmed:copyrightInfo | © 2011 Blackwell Publishing Ltd. | lld:pubmed |
pubmed-article:21689085 | pubmed:issnType | Electronic | lld:pubmed |
pubmed-article:21689085 | pubmed:volume | 154 | lld:pubmed |
pubmed-article:21689085 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:21689085 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:21689085 | pubmed:pagination | 457-65 | lld:pubmed |
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pubmed-article:21689085 | pubmed:year | 2011 | lld:pubmed |
pubmed-article:21689085 | pubmed:articleTitle | Tyrosine kinase inhibitor insensitivity of non-cycling CD34+ human acute myeloid leukaemia cells with FMS-like tyrosine kinase 3 mutations. | lld:pubmed |
pubmed-article:21689085 | pubmed:affiliation | Section of Haemato-Oncology, The Institute of Cancer Research, Sutton, Surrey Department of Clinical Cytogenetics, The Royal Marsden Hospital, Sutton, Surrey. Caroline.Alvares@icr.ac.uk | lld:pubmed |
pubmed-article:21689085 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:21689085 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |