Evidence map›Paper›PMID 20805474›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2010

Isolation and killing of candidate chronic myeloid leukemia stem cells by antibody targeting of IL-1 receptor accessory protein.

Marcus Järås, Petra Johnels, Nils Hansen, Helena Agerstam, Panagiotis Tsapogas, Marianne Rissler, Carin Lassen, Tor Olofsson, Ole Weis Bjerrum, Johan Richter and 1 more

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 104 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
104citing papers in PubMed, 1 pooled it
4.3field-weighted citation impact, top 5% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

104 citing papers in PubMed, 1 synthesis or guideline pooled it, 193 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. TheHematology reports · 2026
    Article
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  5. Review
  6. Article
  7. Article
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  10. Novel targeted therapies in chronic myeloid leukemia.Pharmaceutical science advances · 2024
    Review
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44 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors at 5 institutions in 4 countries.

Marcus JäråsDepartment of Clinical Genetics, University and Regional Laboratories, Skåne University Hospital, Lund University, 22185 Lund, Sweden.
Petra Johnels
Nils Hansen
Helena Agerstam
Panagiotis Tsapogas
Marianne Rissler
Carin Lassen
Tor Olofsson
Ole Weis Bjerrum
Johan Richter
Thoas Fioretos
Lund University · SESkåne University Hospital · SEGene Therapy Laboratory · FRInstitute for Transfusion Medicine · USRigshospitalet · DK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

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.

Indexed as

ApoptosisADP-ribosyl Cyclase 1AntibodiesAntigens, CD34Cell SeparationFusion Proteins, bcr-ablGene Expression ProfilingGene Expression Regulation, NeoplasticHumansInterleukin-1 Receptor Accessory ProteinLeukemia, Myelogenous, Chronic, BCR-ABL PositiveMembrane GlycoproteinsNeoplastic Stem CellsADP-ribosyl Cyclase 1AntibodiesAntigens, CD34CD38 protein, humanFusion Proteins, bcr-ablIL1RAP protein, humanInterleukin-1 Receptor Accessory ProteinMembrane Glycoproteins

Identifiers

PMID20805474
PMCPMC2941341
OpenAlexW2050184823

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.