Evidence map›Paper›PMID 28487542›Full record

ArticleLeukemia2017

Abundant and equipotent founder cells establish and maintain acute lymphoblastic leukaemia.

A Elder, S Bomken, I Wilson, H J Blair, S Cockell, F Ponthan, K Dormon, D Pal, O Heidenreich, J Vormoor

Open access · hybridAbstract read
In one paragraph

Article in Leukemia, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.3field-weighted citation impact, top 22% 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

22 citing papers in PubMed, 53 citations in OpenAlex.

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  12. Interrogation of clonal tracking data usingNature computational science · 2021
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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

10 authors at 2 institutions in 1 country.

A ElderWolfson Childhood Cancer Research Centre, Northern Institute for Cancer Research, Newcastle University, Newcastle upon Tyne, UK.
S BomkenWolfson Childhood Cancer Research Centre, Northern Institute for Cancer Research, Newcastle University, Newcastle upon Tyne, UK.ORCID 0000-0001-9163-5738
I WilsonInstitute of Genetic Medicine, Newcastle University, Newcastle upon Tyne, UK.
H J BlairWolfson Childhood Cancer Research Centre, Northern Institute for Cancer Research, Newcastle University, Newcastle upon Tyne, UK.
S CockellBioinformatics Support Unit, Newcastle University, Newcastle upon Tyne, UK.
F PonthanWolfson Childhood Cancer Research Centre, Northern Institute for Cancer Research, Newcastle University, Newcastle upon Tyne, UK.
K DormonWolfson Childhood Cancer Research Centre, Northern Institute for Cancer Research, Newcastle University, Newcastle upon Tyne, UK.
D PalWolfson Childhood Cancer Research Centre, Northern Institute for Cancer Research, Newcastle University, Newcastle upon Tyne, UK.
O HeidenreichWolfson Childhood Cancer Research Centre, Northern Institute for Cancer Research, Newcastle University, Newcastle upon Tyne, UK.ORCID 0000-0001-5404-6483
J VormoorWolfson Childhood Cancer Research Centre, Northern Institute for Cancer Research, Newcastle University, Newcastle upon Tyne, UK.
Newcastle University · GBNewcastle upon Tyne Hospitals NHS Foundation Trust · GB

Funding

Cancer Research UK 12788Cancer Research UK 23389Cancer Research UK A12788Medical Research Council G0802259National Centre for the Replacement, Refinement and Reduction of Animals in Research NC/P002412/1Wellcome Trust
6 · The paper itself

Abstract

High frequencies of blasts in primary acute lymphoblastic leukaemia (ALL) samples have the potential to induce leukaemia and to engraft mice. However, it is unclear how individual ALL cells each contribute to drive leukaemic development in a bulk transplant and the extent to which these blasts vary functionally. We used cellular barcoding as a fate mapping tool to track primograft ALL blasts in vivo. Our results show that high numbers of ALL founder cells contribute at similar frequencies to leukaemic propagation over serial transplants, without any clear evidence of clonal succession. These founder cells also exhibit equal capacity to home and engraft to different organs, although stochastic processes may alter the composition in restrictive niches. Our findings enhance the stochastic stem cell model of ALL by demonstrating equal functional abilities of singular ALL blasts and show that successful treatment strategies must eradicate the entire leukaemic cell population.

Indexed as

Biomarkers, TumorCell Transformation, NeoplasticAnimalsClonal EvolutionComputational BiologyDisease Models, AnimalGene Expression ProfilingHeterograftsHigh-Throughput Nucleotide SequencingHumansMiceModels, BiologicalNeoplastic Stem CellsPrecursor Cell Lymphoblastic Leukemia-LymphomaBiomarkers, Tumor

Identifiers

PMID28487542
PMCPMC5558874
OpenAlexW2613468286

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.