Evidence map›Paper›PMID 28122740›Full record

ArticleBlood2017

Single-cell molecular analysis defines therapy response and immunophenotype of stem cell subpopulations in CML.

Rebecca Warfvinge, Linda Geironson, Mikael N E Sommarin, Stefan Lang, Christine Karlsson, Teona Roschupkina, Leif Stenke, Jesper Stentoft, Ulla Olsson-Strömberg, Henrik Hjorth-Hansen and 4 more

Open access · bronzeAbstract read
In one paragraph

Article in Blood, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
84citing papers in PubMed, 1 pooled it
16.9field-weighted citation impact, top 1% 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

84 citing papers in PubMed, 1 synthesis or guideline pooled it, 177 citations in OpenAlex.

  1. Pooled it
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  12. Novel targeted therapies in chronic myeloid leukemia.Pharmaceutical science advances · 2024
    Review
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  15. Article
  16. Cancer Stem Cells from Definition to Detection and Targeted Drugs.International journal of molecular sciences · 2024
    Review
  17. Article
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  19. Review
  20. Review

24 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

14 authors at 6 institutions in 4 countries.

Rebecca WarfvingeDivision of Molecular Hematology, and.
Linda GeironsonDivision of Molecular Hematology, and.
Mikael N E SommarinDivision of Molecular Hematology, and.ORCID 0000-0002-2581-5543
Stefan LangDivision of Molecular Hematology, and.
Christine KarlssonDivision of Molecular Medicine and Gene Therapy, Lund Stem Cell Center, Lund University, Lund, Sweden.
Teona RoschupkinaDivision of Molecular Hematology, and.
Leif StenkeDepartment of Hematology, Karolinska University Hospital, Stockholm, Sweden.
Jesper StentoftDepartment of Hematology, Aarhus University Hospital, Aarhus, Denmark.
Ulla Olsson-StrömbergDepartment of Medical Science, and.
Henrik Hjorth-HansenDepartment of Hematology, St. Olavs Hospital, Trondheim, Norway.
Satu MustjokiHematology Research Unit Helsinki and Department of Clinical Chemistry, University of Helsinki, Helsinki, Finland.
Shamit SonejiDivision of Molecular Hematology, and.
Johan RichterDivision of Molecular Medicine and Gene Therapy, Lund Stem Cell Center, Lund University, Lund, Sweden.
Göran KarlssonDivision of Molecular Hematology, and.
Lund University · SEAarhus University Hospital · DKKarolinska University Hospital · SENorwegian University of Science and Technology · NOUniversity of Helsinki · FIUppsala University Hospital · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Understanding leukemia heterogeneity is critical for the development of curative treatments as the failure to eliminate therapy-persistent leukemic stem cells (LSCs) may result in disease relapse. Here we have combined high-throughput immunophenotypic screens with large-scale single-cell gene expression analysis to define the heterogeneity within the LSC population in chronic phase chronic myeloid leukemia (CML) patients at diagnosis and following conventional tyrosine kinase inhibitor (TKI) treatment. Our results reveal substantial heterogeneity within the putative LSC population in CML at diagnosis and demonstrate differences in response to subsequent TKI treatment between distinct subpopulations. Importantly, LSC subpopulations with myeloid and proliferative molecular signatures are proportionally reduced at a higher extent in response to TKI therapy compared with subfractions displaying primitive and quiescent signatures. Additionally, cell surface expression of the CML stem cell markers CD25, CD26, and IL1RAP is high in all subpopulations at diagnosis but downregulated and unevenly distributed across subpopulations in response to TKI treatment. The most TKI-insensitive cells of the LSC compartment can be captured within the CD45RA

Indexed as

ADP-ribosyl Cyclase 1Antigens, CD34Antineoplastic AgentsBiomarkers, TumorCase-Control StudiesCell LineageDipeptidyl Peptidase 4Gene ExpressionGenetic HeterogeneityHumansImmunophenotypingInterleukin-1 Receptor Accessory ProteinInterleukin-2 Receptor alpha SubunitLeukemia, Myelogenous, Chronic, BCR-ABL PositiveLeukocyte Common AntigensNeoplastic Stem CellsADP-ribosyl Cyclase 1Antigens, CD34Antineoplastic AgentsBiomarkers, TumorDipeptidyl Peptidase 4DPP4 protein, humanIL1RAP protein, humanIL2RA protein, humanInterleukin-1 Receptor Accessory ProteinInterleukin-2 Receptor alpha SubunitLeukocyte Common AntigensProtein Kinase InhibitorsProto-Oncogene Proteins c-kit

Identifiers

PMID28122740
PMCPMC5484462
OpenAlexW2580232087

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.