Evidence map›Paper›PMID 35108372›Full record

ArticleBlood2022

Molecular characterization of mutant TP53 acute myeloid leukemia and high-risk myelodysplastic syndrome.

Tim Grob, Adil S A Al Hinai, Mathijs A Sanders, François G Kavelaars, Melissa Rijken, Patrycja L Gradowska, Bart J Biemond, Dimitri A Breems, Johan Maertens, Marinus van Marwijk Kooy and 10 more

Open access · hybridAbstract read
In one paragraph

Article in Blood, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 185 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
185citing papers in PubMed, 2 pooled it
41.9field-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

185 citing papers in PubMed, 2 syntheses or guidelines pooled it, 276 citations in OpenAlex.

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  3. Treatment ofHaematologica · 2026
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125 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

20 authors at 10 institutions in 4 countries.

Tim GrobDepartment of Hematology, Erasmus MC Cancer Institute, University Medical Center Rotterdam, Rotterdam, The Netherlands.
Adil S A Al HinaiDepartment of Hematology, Erasmus MC Cancer Institute, University Medical Center Rotterdam, Rotterdam, The Netherlands.
Mathijs A SandersDepartment of Hematology, Erasmus MC Cancer Institute, University Medical Center Rotterdam, Rotterdam, The Netherlands.ORCID 0000-0002-8575-9213
François G KavelaarsDepartment of Hematology, Erasmus MC Cancer Institute, University Medical Center Rotterdam, Rotterdam, The Netherlands.
Melissa RijkenDepartment of Hematology, Erasmus MC Cancer Institute, University Medical Center Rotterdam, Rotterdam, The Netherlands.
Patrycja L GradowskaDepartment of Hematology, Erasmus MC Cancer Institute, University Medical Center Rotterdam, Rotterdam, The Netherlands.ORCID 0000-0002-4620-9163
Bart J BiemondDepartment of Hematology, Amsterdam University Medical Center, Amsterdam, The Netherlands.ORCID 0000-0002-4426-5743
Dimitri A BreemsDepartment of Hematology, Ziekenhuis Netwerk Antwerpen, Antwerp, Belgium.
Johan MaertensDepartment of Hematology, University Hospital Gasthuisberg, Leuven, Belgium.
Marinus van Marwijk KooyDepartment of Hematology, Isala Hospital, Zwolle, The Netherlands.
Thomas PabstDepartment of Oncology, University Hospital, Inselspital, Bern, Switzerland.
Okke de WeerdtDepartment of Hematology, Saint Antonius Hospital, Nieuwegein, The Netherlands.
Gert J OssenkoppeleDepartment of Hematology, Amsterdam University Medical Center, Amsterdam, The Netherlands.
Arjan A van de LoosdrechtDepartment of Hematology, Amsterdam University Medical Center, Amsterdam, The Netherlands.
Gerwin A HulsDepartment of Hematology, University Medical Center Groningen, Groningen, The Netherlands; and.
Jan J CornelissenDepartment of Hematology, Erasmus MC Cancer Institute, University Medical Center Rotterdam, Rotterdam, The Netherlands.
H Berna BeverlooDepartment of Clinical Genetics, University Medical Center Rotterdam, Rotterdam, The Netherlands.
Bob LöwenbergDepartment of Hematology, Erasmus MC Cancer Institute, University Medical Center Rotterdam, Rotterdam, The Netherlands.ORCID 0000-0001-8982-5217
Mojca Jongen-LavrencicDepartment of Hematology, Erasmus MC Cancer Institute, University Medical Center Rotterdam, Rotterdam, The Netherlands.
Peter J M ValkDepartment of Hematology, Erasmus MC Cancer Institute, University Medical Center Rotterdam, Rotterdam, The Netherlands.ORCID 0000-0002-8857-9461
Erasmus MC Cancer Institute · NLAmsterdam University Medical Centers · NLIsala · NLMinistry of Health · OMRotterdam University of Applied Sciences · NLSt. Antonius Ziekenhuis · NLUniversitair Ziekenhuis Leuven · BEUniversity Hospital of Bern · CHUniversity Medical Center Groningen · NLZiekenhuisnetwerk Antwerpen Stuivenberg · BE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Substantial heterogeneity within mutant TP53 acute myeloid leukemia (AML) and myelodysplastic syndrome with excess of blast (MDS-EB) precludes the exact assessment of prognostic impact for individual patients. We performed in-depth clinical and molecular analysis of mutant TP53 AML and MDS-EB to dissect the molecular characteristics in detail and determine its impact on survival. We performed next-generation sequencing on 2200 AML/MDS-EB specimens and assessed the TP53 mutant allelic status (mono- or bi-allelic), the number of TP53 mutations, mutant TP53 clone size, concurrent mutations, cytogenetics, and mutant TP53 molecular minimal residual disease and studied the associations of these characteristics with overall survival. TP53 mutations were detected in 230 (10.5%) patients with AML/MDS-EB with a median variant allele frequency of 47%. Bi-allelic mutant TP53 status was observed in 174 (76%) patients. Multiple TP53 mutations were found in 49 (21%) patients. Concurrent mutations were detected in 113 (49%) patients. No significant difference in any of the aforementioned molecular characteristics of mutant TP53 was detected between AML and MDS-EB. Patients with mutant TP53 have a poor outcome (2-year overall survival, 12.8%); however, no survival difference between AML and MDS-EB was observed. Importantly, none of the molecular characteristics were significantly associated with survival in mutant TP53 AML/MDS-EB. In most patients, TP53 mutations remained detectable in complete remission by deep sequencing (73%). Detection of residual mutant TP53 was not associated with survival. Mutant TP53 AML and MDS-EB do not differ with respect to molecular characteristics and survival. Therefore, mutant TP53 AML/MDS-EB should be considered a distinct molecular disease entity.

Indexed as

Leukemia, Myeloid, AcuteMyelodysplastic SyndromesCytogeneticsHumansMutationTumor Suppressor Protein p53TP53 protein, humanTumor Suppressor Protein p53

Identifiers

PMID35108372
PMCPMC11022827
OpenAlexW4210694051

What OpenQuestion holds

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LicenceCC BY-NC-ND
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.