Evidence map›Paper›PMID 30755419›Full record

ArticleBlood2019

Altered NFE2 activity predisposes to leukemic transformation and myelosarcoma with AML-specific aberrations.

Jonas Samuel Jutzi, Titiksha Basu, Maximilian Pellmann, Sandra Kaiser, Doris Steinemann, Mathijs A Sanders, Adil S A Hinai, Annelieke Zeilemaker, Sarolta Bojtine Kovacs, Christoph Koellerer and 9 more

Open access · bronzeAbstract read
In one paragraph

Article in Blood, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

25 citing papers in PubMed, 38 citations in OpenAlex.

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  12. Diagnostic Approaches in Myeloid Sarcoma.Current issues in molecular biology · 2025
    Review
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  19. 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

19 authors at 6 institutions in 3 countries.

Jonas Samuel JutziSection of Molecular Hematology, Department of Medicine I, Hematology, Oncology and Stem Cell Transplantation, University Medical Center Freiburg, Faculty of Medicine, University of Freiburg, Freiburg, Germany.ORCID 0000-0002-1977-153X
Titiksha BasuSection of Molecular Hematology, Department of Medicine I, Hematology, Oncology and Stem Cell Transplantation, University Medical Center Freiburg, Faculty of Medicine, University of Freiburg, Freiburg, Germany.
Maximilian PellmannSection of Molecular Hematology, Department of Medicine I, Hematology, Oncology and Stem Cell Transplantation, University Medical Center Freiburg, Faculty of Medicine, University of Freiburg, Freiburg, Germany.
Sandra KaiserSection of Molecular Hematology, Department of Medicine I, Hematology, Oncology and Stem Cell Transplantation, University Medical Center Freiburg, Faculty of Medicine, University of Freiburg, Freiburg, Germany.
Doris SteinemannDepartment of Human Genetics, Hannover Medical School, Hannover, Germany.ORCID 0000-0001-8797-0816
Mathijs A SandersDepartment of Hematology, Erasmus MC Cancer Institute, Rotterdam, The Netherlands.ORCID 0000-0002-8575-9213
Adil S A HinaiDepartment of Hematology, Erasmus MC Cancer Institute, Rotterdam, The Netherlands.ORCID 0000-0002-1118-017X
Annelieke ZeilemakerDepartment of Hematology, Erasmus MC Cancer Institute, Rotterdam, The Netherlands.
Sarolta Bojtine KovacsSection of Molecular Hematology, Department of Medicine I, Hematology, Oncology and Stem Cell Transplantation, University Medical Center Freiburg, Faculty of Medicine, University of Freiburg, Freiburg, Germany.
Christoph KoellererSection of Molecular Hematology, Department of Medicine I, Hematology, Oncology and Stem Cell Transplantation, University Medical Center Freiburg, Faculty of Medicine, University of Freiburg, Freiburg, Germany.
Jenny OstendorpSection of Molecular Hematology, Department of Medicine I, Hematology, Oncology and Stem Cell Transplantation, University Medical Center Freiburg, Faculty of Medicine, University of Freiburg, Freiburg, Germany.
Konrad AumannInstitute for Surgical Pathology, University Medical Center Freiburg, Faculty of Medicine, University of Freiburg, Freiburg, Germany.ORCID 0000-0001-8178-1571
Wei WangSection of Molecular Hematology, Department of Medicine I, Hematology, Oncology and Stem Cell Transplantation, University Medical Center Freiburg, Faculty of Medicine, University of Freiburg, Freiburg, Germany.
Emmanuel RaffouxHôpital Saint-Louis, Paris 7 University, Service d'Hématologie Adulte, Assistance Publique-Hôpitaux de Paris (APHP), Paris, France.
Bruno CassinatAPHP, Hôpital Saint-Louis, Laboratoire de Biologie Cellulaire, Paris, France.ORCID 0000-0002-6514-3905
Lars BullingerDepartment of Internal Medicine III, University Hospital of Ulm, Ulm, Germany; and.ORCID 0000-0002-5890-5510
Brigitte SchlegelbergerDepartment of Human Genetics, Hannover Medical School, Hannover, Germany.ORCID 0000-0001-5256-1270
Peter J M ValkDepartment of Hematology, Erasmus MC Cancer Institute, Rotterdam, The Netherlands.
Heike Luise PahlSection of Molecular Hematology, Department of Medicine I, Hematology, Oncology and Stem Cell Transplantation, University Medical Center Freiburg, Faculty of Medicine, University of Freiburg, Freiburg, Germany.ORCID 0000-0003-2857-2396
University of Freiburg · DEErasmus MC Cancer Institute · NLMedizinische Hochschule Hannover · DEAssistance Publique – Hôpitaux de Paris · FRUniversité Paris Cité · FRUniversity Hospital Ulm · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In acute myeloid leukemia (AML), acquired genetic aberrations carry prognostic implications and guide therapeutic decisions. Clinical algorithms have been improved by the incorporation of novel aberrations. Here, we report the presence and functional characterization of mutations in the transcription factor NFE2 in patients with AML and in a patient with myelosarcoma. We previously described NFE2 mutations in patients with myeloproliferative neoplasms and demonstrated that expression of mutant NFE2 in mice causes a myeloproliferative phenotype. Now, we show that, during follow-up, 34% of these mice transform to leukemia presenting with or without concomitant myelosarcomas, or develop isolated myelosarcomas. These myelosarcomas and leukemias acquired AML-specific alterations, including the murine equivalent of trisomy 8, loss of the AML commonly deleted region on chromosome 5q, and mutations in the tumor suppressor

Indexed as

AdolescentAdultAgedAged, 80 and overAnimalsCell Transformation, NeoplasticChromosome AberrationsFemaleHumansLeukemia, Myeloid, AcuteMaleMiceMiddle AgedMutationNF-E2 Transcription Factor, p45 SubunitSarcoma, MyeloidNFE2 protein, humanNfe2 protein, mouseNF-E2 Transcription Factor, p45 SubunitTumor Suppressor Protein p53

Identifiers

PMID30755419
PMCPMC6484461
OpenAlexW2912086620

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.