Evidence map›Paper›PMID 32024830›Full record

ArticleNature communications2020

Clonal competition within complex evolutionary hierarchies shapes AML over time.

Carl Sandén, Henrik Lilljebjörn, Christina Orsmark Pietras, Rasmus Henningsson, Karim H Saba, Niklas Landberg, Hanna Thorsson, Sofia von Palffy, Pablo Peña-Martinez, Carl Högberg and 6 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 1 pooled it
2.7field-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

23 citing papers in PubMed, 1 synthesis or guideline pooled it, 26 citations in OpenAlex.

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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

16 authors at 2 institutions in 1 country.

Carl SandénDivision of Clinical Genetics, Department of Laboratory Medicine, Lund University, Lund, Sweden. carl.sanden@med.lu.se.ORCID http://orcid.org/0000-0002-8931-9565
Henrik LilljebjörnDivision of Clinical Genetics, Department of Laboratory Medicine, Lund University, Lund, Sweden.ORCID http://orcid.org/0000-0001-8703-1173
Christina Orsmark PietrasDivision of Clinical Genetics, Department of Laboratory Medicine, Lund University, Lund, Sweden.
Rasmus HenningssonDivision of Clinical Genetics, Department of Laboratory Medicine, Lund University, Lund, Sweden.
Karim H SabaDivision of Clinical Genetics, Department of Laboratory Medicine, Lund University, Lund, Sweden.ORCID http://orcid.org/0000-0003-4946-6488
Niklas LandbergDivision of Clinical Genetics, Department of Laboratory Medicine, Lund University, Lund, Sweden.ORCID http://orcid.org/0000-0001-6752-6507
Hanna ThorssonDivision of Clinical Genetics, Department of Laboratory Medicine, Lund University, Lund, Sweden.
Sofia von PalffyDivision of Clinical Genetics, Department of Laboratory Medicine, Lund University, Lund, Sweden.ORCID http://orcid.org/0000-0001-5640-4037
Pablo Peña-MartinezDivision of Clinical Genetics, Department of Laboratory Medicine, Lund University, Lund, Sweden.ORCID http://orcid.org/0000-0002-0789-6431
Carl HögbergDivision of Clinical Genetics, Department of Laboratory Medicine, Lund University, Lund, Sweden.
Marianne RisslerDivision of Clinical Genetics, Department of Laboratory Medicine, Lund University, Lund, Sweden.
David GisselssonDivision of Clinical Genetics, Department of Laboratory Medicine, Lund University, Lund, Sweden.ORCID http://orcid.org/0000-0002-0301-426X
Vladimir LazarevicDepartment of Hematology, Oncology and Radiation Physics, Skåne University Hospital, Lund, Sweden.ORCID http://orcid.org/0000-0002-1782-4423
Gunnar JuliussonDepartment of Hematology, Oncology and Radiation Physics, Skåne University Hospital, Lund, Sweden.
Helena ÅgerstamDivision of Clinical Genetics, Department of Laboratory Medicine, Lund University, Lund, Sweden.
Thoas FioretosDivision of Clinical Genetics, Department of Laboratory Medicine, Lund University, Lund, Sweden. thoas.fioretos@med.lu.se.
Lund University · SESkåne University Hospital · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Clonal heterogeneity and evolution has major implications for disease progression and relapse in acute myeloid leukemia (AML). To model clonal dynamics in vivo, we serially transplanted 23 AML cases to immunodeficient mice and followed clonal composition for up to 15 months by whole-exome sequencing of 84 xenografts across two generations. We demonstrate vast changes in clonality that both progress and reverse over time, and define five patterns of clonal dynamics: Monoclonal, Stable, Loss, Expansion and Burst. We also show that subclonal expansion in vivo correlates with a more adverse prognosis. Furthermore, clonal expansion enabled detection of very rare clones with AML driver mutations that were undetectable by sequencing at diagnosis, demonstrating that the vast majority of AML cases harbor multiple clones already at diagnosis. Finally, the rise and fall of related clones enabled deconstruction of the complex evolutionary hierarchies of the clones that compete to shape AML over time.

Indexed as

Clonal EvolutionAdultAgedAged, 80 and overAnimalsDisease ProgressionExome SequencingFemaleHumansLeukemia, Myeloid, AcuteMaleMiceMiddle AgedMutation

Identifiers

PMID32024830
PMCPMC7002407
OpenAlexW3005125447

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.