Evidence map›Paper›PMID 31907378›Full record

ReviewNature reviews. Cancer2020

The leukaemia stem cell: similarities, differences and clinical prospects in CML and AML.

David Vetrie, G Vignir Helgason, Mhairi Copland

Open access · greenAbstract readHistorical ArticleReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Cancer, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 193 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
193citing papers in PubMed, 1 pooled it
30.2field-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

193 citing papers in PubMed, 1 synthesis or guideline pooled it, 363 citations in OpenAlex.

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133 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

3 authors at 2 institutions in 1 country.

David VetrieWolfson Wohl Cancer Research Centre, Institute of Cancer Sciences, University of Glasgow, Glasgow, UK. david.vetrie@glasgow.ac.uk.ORCID http://orcid.org/0000-0003-2075-4662
G Vignir HelgasonWolfson Wohl Cancer Research Centre, Institute of Cancer Sciences, University of Glasgow, Glasgow, UK.ORCID http://orcid.org/0000-0003-1616-132X
Mhairi CoplandPaul O'Gorman Leukaemia Research Centre, Institute of Cancer Sciences, University of Glasgow, Glasgow, UK. mhairi.copland@glasgow.ac.uk.ORCID http://orcid.org/0000-0002-7655-016X
University of Glasgow · GBBlood Cancer UK · GB

Funding

Cancer Research UK 24896Cancer Research UK 29754Cancer Research UK C55731/A24896
6 · The paper itself

Abstract

For two decades, leukaemia stem cells (LSCs) in chronic myeloid leukaemia (CML) and acute myeloid leukaemia (AML) have been advanced paradigms for the cancer stem cell field. In CML, the acquisition of the fusion tyrosine kinase BCR-ABL1 in a haematopoietic stem cell drives its transformation to become a LSC. In AML, LSCs can arise from multiple cell types through the activity of a number of oncogenic drivers and pre-leukaemic events, adding further layers of context and genetic and cellular heterogeneity to AML LSCs not observed in most cases of CML. Furthermore, LSCs from both AML and CML can be refractory to standard-of-care therapies and persist in patients, diversify clonally and serve as reservoirs to drive relapse, recurrence or progression to more aggressive forms. Despite these complexities, LSCs in both diseases share biological features, making them distinct from other CML or AML progenitor cells and from normal haematopoietic stem cells. These features may represent Achilles' heels against which novel therapies can be developed. Here, we review many of the similarities and differences that exist between LSCs in CML and AML and examine the therapeutic strategies that could be used to eradicate them.

Indexed as

AnimalsBiomarkers, TumorCell Transformation, NeoplasticDisease ManagementDisease SusceptibilityDrug DevelopmentHistory, 20th CenturyHistory, 21st CenturyHumansLeukemia, Myelogenous, Chronic, BCR-ABL PositiveLeukemia, Myeloid, AcuteMolecular Targeted TherapyNeoplastic Stem CellsResearchBiomarkers, Tumor

Identifiers

PMID31907378
OpenAlexW2998012982

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.