Evidence map›Paper›PMID 35027675›Full record

ArticleBone marrow transplantation2022

Clonal evolution in patients developing therapy-related myeloid neoplasms following autologous stem cell transplantation.

Johannes Frasez Soerensen, Anni Aggerholm, Carina Agerbo Rosenberg, Marie Bill, Gitte Birk Kerndrup, Lene Hyldahl Ebbesen, Marcus Høy Hansen, Anne Stidsholt Roug, Maja Ludvigsen

Abstract read
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In one paragraph

Article in Bone marrow transplantation, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed, 2 pooled it
1.8field-weighted citation impact, top 14% 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

11 citing papers in PubMed, 2 syntheses or guidelines pooled it, 12 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
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  6. Gene therapy for the leukodystrophies: From preclinical animal studies to clinical trials.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2024
    Review
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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

9 authors at 2 institutions in 1 country.

Johannes Frasez SoerensenDepartment of Hematology, Aarhus University Hospital, Aarhus, Denmark. johasr@rm.dk.ORCID http://orcid.org/0000-0002-4404-0835
Anni AggerholmDepartment of Hematology, Aarhus University Hospital, Aarhus, Denmark.ORCID http://orcid.org/0000-0002-8915-0122
Carina Agerbo RosenbergDepartment of Hematology, Aarhus University Hospital, Aarhus, Denmark.
Marie BillDepartment of Hematology, Aarhus University Hospital, Aarhus, Denmark.
Gitte Birk KerndrupDepartment of Pathology, Aarhus University Hospital, Aarhus, Denmark.
Lene Hyldahl EbbesenDepartment of Hematology, Aarhus University Hospital, Aarhus, Denmark.
Marcus Høy HansenDepartment of Hematology, Aarhus University Hospital, Aarhus, Denmark.
Anne Stidsholt Roug *Department of Hematology, Aarhus University Hospital, Aarhus, Denmark.
Maja Ludvigsen *Department of Hematology, Aarhus University Hospital, Aarhus, Denmark.ORCID http://orcid.org/0000-0001-5089-3271
Aarhus University Hospital · DKAarhus University · DK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Clonal hematopoiesis (CH) denotes somatic mutations in genes related to myeloid neoplasms present at any variant allele frequency (VAF). Clonal hematopoiesis is associated with increasing age and with a factor 6 increase in the risk of developing therapy-related myeloid neoplasms (tMNs) following autologous stem cell transplantation (ASCT). However, the impact of specific mutations on progression from CH to tMN has yet to be unraveled, and it remains unclear whether mutations directly impact or even drive the development of tMN. We performed deep sequencing in longitudinal samples from a cohort of 12 patients with either multiple myeloma or lymphoma who developed tMN following ASCT. Nine patients had one or more mutations that could be tracked longitudinally. Seven patients had clonal expansion from time of ASCT to diagnosis of tMN. Of these, six patients had CH at VAF < 2% at baseline. The median VAF of non-DNMT3A clones increased from 1% (IQR 0.7%-10.0%) at time of ASCT to 37% (IQR 17%-47%) at tMN diagnosis (P = 0.002), while DNMT3A clones showed quiescent trajectories (P = 0.625). Our data provide evidence to support the hypothesis that the development of tMN following ASCT is likely instigated by CH present at VAFs as low as 0.5%, detectable years before tMN onset.

Indexed as

Hematopoietic Stem Cell TransplantationMyeloproliferative DisordersNeoplasms, Second PrimaryClonal EvolutionHumansMutationTransplantation, Autologous

Identifiers

PMID35027675
OpenAlexW4206223587

What OpenQuestion holds

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Registered trials

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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.