| pubmed-article:20805474 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:20805474 | lifeskim:mentions | umls-concept:C0023473 | lld:lifeskim |
| pubmed-article:20805474 | lifeskim:mentions | umls-concept:C0280141 | lld:lifeskim |
| pubmed-article:20805474 | lifeskim:mentions | umls-concept:C0033684 | lld:lifeskim |
| pubmed-article:20805474 | lifeskim:mentions | umls-concept:C0003241 | lld:lifeskim |
| pubmed-article:20805474 | lifeskim:mentions | umls-concept:C0063710 | lld:lifeskim |
| pubmed-article:20805474 | lifeskim:mentions | umls-concept:C0204727 | lld:lifeskim |
| pubmed-article:20805474 | lifeskim:mentions | umls-concept:C0205409 | lld:lifeskim |
| pubmed-article:20805474 | lifeskim:mentions | umls-concept:C1378511 | lld:lifeskim |
| pubmed-article:20805474 | lifeskim:mentions | umls-concept:C0599894 | lld:lifeskim |
| pubmed-article:20805474 | lifeskim:mentions | umls-concept:C0162388 | lld:lifeskim |
| pubmed-article:20805474 | pubmed:issue | 37 | lld:pubmed |
| pubmed-article:20805474 | pubmed:dateCreated | 2010-9-15 | lld:pubmed |
| pubmed-article:20805474 | pubmed:abstractText | Chronic myeloid leukemia (CML) is genetically characterized by the Philadelphia (Ph) chromosome, formed through a reciprocal translocation between chromosomes 9 and 22 and giving rise to the constitutively active tyrosine kinase P210 BCR/ABL1. Therapeutic strategies aiming for a cure of CML will require full eradication of Ph chromosome-positive (Ph(+)) CML stem cells. Here we used gene-expression profiling to identify IL-1 receptor accessory protein (IL1RAP) as up-regulated in CML CD34(+) cells and also in cord blood CD34(+) cells as a consequence of retroviral BCR/ABL1 expression. To test whether IL1RAP expression distinguishes normal (Ph(-)) and leukemic (Ph(+)) cells within the CML CD34(+)CD38(-) cell compartment, we established a unique protocol for conducting FISH on small numbers of sorted cells. By using this method, we sorted cells directly into drops on slides to investigate their Ph-chromosome status. Interestingly, we found that the CML CD34(+)CD38(-)IL1RAP(+) cells were Ph(+), whereas CML CD34(+)CD38(-)IL1RAP(-) cells were almost exclusively Ph(-). By performing long-term culture-initiating cell assays on the two cell populations, we found that Ph(+) and Ph(-) candidate CML stem cells could be prospectively separated. In addition, by generating an anti-IL1RAP antibody, we provide proof of concept that IL1RAP can be used as a target on CML CD34(+)CD38(-) cells to induce antibody-dependent cell-mediated cytotoxicity. This study thus identifies IL1RAP as a unique cell surface biomarker distinguishing Ph(+) from Ph(-) candidate CML stem cells and opens up a previously unexplored avenue for therapy of CML. | lld:pubmed |
| pubmed-article:20805474 | pubmed:language | eng | lld:pubmed |
| pubmed-article:20805474 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:20805474 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:20805474 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:20805474 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:20805474 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:20805474 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:20805474 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:20805474 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:20805474 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:20805474 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:20805474 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:20805474 | pubmed:month | Sep | lld:pubmed |
| pubmed-article:20805474 | pubmed:issn | 1091-6490 | lld:pubmed |
| pubmed-article:20805474 | pubmed:author | pubmed-author:FioretosThoas... | lld:pubmed |
| pubmed-article:20805474 | pubmed:author | pubmed-author:RichterJohanJ | lld:pubmed |
| pubmed-article:20805474 | pubmed:author | pubmed-author:OlofssonTorT | lld:pubmed |
| pubmed-article:20805474 | pubmed:author | pubmed-author:LassenCarinC | lld:pubmed |
| pubmed-article:20805474 | pubmed:author | pubmed-author:AgerstamHelen... | lld:pubmed |
| pubmed-article:20805474 | pubmed:author | pubmed-author:TsapogasPanag... | lld:pubmed |
| pubmed-article:20805474 | pubmed:author | pubmed-author:BjerrumOle... | lld:pubmed |
| pubmed-article:20805474 | pubmed:author | pubmed-author:HansenNilsN | lld:pubmed |
| pubmed-article:20805474 | pubmed:author | pubmed-author:JäråsMarcusM | lld:pubmed |
| pubmed-article:20805474 | pubmed:author | pubmed-author:JohnelsPetraP | lld:pubmed |
| pubmed-article:20805474 | pubmed:author | pubmed-author:RisslerMarian... | lld:pubmed |
| pubmed-article:20805474 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:20805474 | pubmed:day | 14 | lld:pubmed |
| pubmed-article:20805474 | pubmed:volume | 107 | lld:pubmed |
| pubmed-article:20805474 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:20805474 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:20805474 | pubmed:pagination | 16280-5 | lld:pubmed |
| pubmed-article:20805474 | pubmed:meshHeading | pubmed-meshheading:20805474... | lld:pubmed |
| pubmed-article:20805474 | pubmed:meshHeading | pubmed-meshheading:20805474... | lld:pubmed |
| pubmed-article:20805474 | pubmed:meshHeading | pubmed-meshheading:20805474... | lld:pubmed |
| pubmed-article:20805474 | pubmed:meshHeading | pubmed-meshheading:20805474... | lld:pubmed |
| pubmed-article:20805474 | pubmed:meshHeading | pubmed-meshheading:20805474... | lld:pubmed |
| pubmed-article:20805474 | pubmed:meshHeading | pubmed-meshheading:20805474... | lld:pubmed |
| pubmed-article:20805474 | pubmed:meshHeading | pubmed-meshheading:20805474... | lld:pubmed |
| pubmed-article:20805474 | pubmed:meshHeading | pubmed-meshheading:20805474... | lld:pubmed |
| pubmed-article:20805474 | pubmed:meshHeading | pubmed-meshheading:20805474... | lld:pubmed |
| pubmed-article:20805474 | pubmed:meshHeading | pubmed-meshheading:20805474... | lld:pubmed |
| pubmed-article:20805474 | pubmed:meshHeading | pubmed-meshheading:20805474... | lld:pubmed |
| pubmed-article:20805474 | pubmed:meshHeading | pubmed-meshheading:20805474... | lld:pubmed |
| pubmed-article:20805474 | pubmed:meshHeading | pubmed-meshheading:20805474... | lld:pubmed |
| pubmed-article:20805474 | pubmed:year | 2010 | lld:pubmed |
| pubmed-article:20805474 | pubmed:articleTitle | Isolation and killing of candidate chronic myeloid leukemia stem cells by antibody targeting of IL-1 receptor accessory protein. | lld:pubmed |
| pubmed-article:20805474 | pubmed:affiliation | Department of Clinical Genetics, University and Regional Laboratories, Skåne University Hospital, Lund University, 22185 Lund, Sweden. | lld:pubmed |
| pubmed-article:20805474 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:20805474 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| entrez-gene:3556 | entrezgene:pubmed | pubmed-article:20805474 | lld:entrezgene |
| http://linkedlifedata.com/r... | entrezgene:pubmed | pubmed-article:20805474 | lld:entrezgene |
