Evidence map›Paper›PMID 29284680›Full record

ArticleHaematologica2018

CD36 defines primitive chronic myeloid leukemia cells less responsive to imatinib but vulnerable to antibody-based therapeutic targeting.

Niklas Landberg, Sofia von Palffy, Maria Askmyr, Henrik Lilljebjörn, Carl Sandén, Marianne Rissler, Satu Mustjoki, Henrik Hjorth-Hansen, Johan Richter, Helena Ågerstam and 2 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Haematologica, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed, 1 pooled it
3.1field-weighted citation impact, top 8% 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

42 citing papers in PubMed, 1 synthesis or guideline pooled it, 69 citations in OpenAlex.

  1. Pooled it
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  11. Novel targeted therapies in chronic myeloid leukemia.Pharmaceutical science advances · 2024
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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

12 authors at 4 institutions in 3 countries.

Niklas LandbergDivision of Clinical Genetics, Department of Laboratory Medicine, Lund University, Sweden niklas.landberg@med.lu.se thoas.fioretos@med.lu.se.
Sofia von PalffyDivision of Clinical Genetics, Department of Laboratory Medicine, Lund University, Sweden.
Maria AskmyrDivision of Clinical Genetics, Department of Laboratory Medicine, Lund University, Sweden.
Henrik LilljebjörnDivision of Clinical Genetics, Department of Laboratory Medicine, Lund University, Sweden.
Carl SandénDivision of Clinical Genetics, Department of Laboratory Medicine, Lund University, Sweden.
Marianne RisslerDivision of Clinical Genetics, Department of Laboratory Medicine, Lund University, Sweden.
Satu MustjokiHematology Research Unit Helsinki, Department of Clinical Chemistry and Hematology, University of Helsinki, and Helsinki University Hospital Comprehensive Cancer Center, Finland.
Henrik Hjorth-HansenDepartment of Hematology, St Olavs Hospital, Trondheim, Norway.
Johan RichterDepartment of Hematology, Oncology and Radiation Physics, Skåne University Hospital, Lund, Sweden.
Helena ÅgerstamDivision of Clinical Genetics, Department of Laboratory Medicine, Lund University, Sweden.
Marcus JäråsDivision of Clinical Genetics, Department of Laboratory Medicine, Lund University, Sweden.
Thoas FioretosDivision of Clinical Genetics, Department of Laboratory Medicine, Lund University, Sweden niklas.landberg@med.lu.se thoas.fioretos@med.lu.se.
Lund University · SESkåne University Hospital · SESt Olav's University Hospital · NOUniversity of Helsinki · FI

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tyrosine kinase inhibitors (TKIs) are highly effective for the treatment of chronic myeloid leukemia (CML), but very few patients are cured. The major drawbacks regarding TKIs are their low efficacy in eradicating the leukemic stem cells responsible for disease maintenance and relapse upon drug cessation. Herein, we performed ribonucleic acid sequencing of flow-sorted primitive (CD34

Indexed as

Antibody-Dependent Cell CytotoxicityAntibodies, NeoplasmAntigens, NeoplasmCD36 AntigensHumansImatinib MesylateLeukemia, Myeloid, Chronic-PhaseSequence Analysis, RNATumor Cells, CulturedUp-RegulationAntibodies, NeoplasmAntigens, NeoplasmCD36 AntigensImatinib Mesylate

Identifiers

PMID29284680
PMCPMC5830390
OpenAlexW2775901890

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.