Evidence map›Paper›PMID 31867767›Full record

ReviewBioEssays : news and reviews in molecular, cellular and developmental biology2020

Gain-of-Function Effects of N-Terminal CEBPA Mutations in Acute Myeloid Leukemia.

Luisa Schmidt, Elizabeth Heyes, Florian Grebien

Open access · hybridAbstract readReview
In one paragraph

Review in BioEssays : news and reviews in molecular, cellular and developmental biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.0field-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

19 citing papers in PubMed, 27 citations in OpenAlex.

  1. Article
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  6. Frontiers in genetics · 2025
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  18. Zebrafish models of acute leukemias: Current models and future directions.Wiley interdisciplinary reviews. Developmental biology · 2021
    Review
  19. Article
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

3 authors at 1 institution in 1 country.

Luisa SchmidtInstitute for Medical Biochemistry, University of Veterinary Medicine, Vienna, 1210, Austria.
Elizabeth HeyesInstitute for Medical Biochemistry, University of Veterinary Medicine, Vienna, 1210, Austria.
Florian GrebienInstitute for Medical Biochemistry, University of Veterinary Medicine, Vienna, 1210, Austria.ORCID 0000-0003-4289-2281
University of Veterinary Medicine Vienna · AT

Funding

European Research Council 636855
6 · The paper itself

Abstract

Mutations in the CEBPA gene are present in 10-15% of acute myeloid leukemia (AML) patients. The most frequent type of mutations leads to the expression of an N-terminally truncated variant of the transcription factor CCAAT/enhancer-binding protein alpha (C/EBPα), termed p30. While initial reports proposed that p30 represents a dominant-negative version of the wild-type C/EBPα protein, other studies show that p30 retains the capacity to actively regulate gene expression. Recent global transcriptomic and epigenomic analyses have advanced the understanding of the distinct roles of the p30 isoform in leukemogenesis. This review outlines direct and indirect effects of the C/EBPα p30 variant on oncogenic transformation of hematopoietic progenitor cells and discusses how studies of N-terminal CEBPA mutations in AML can be extrapolated to identify novel gain-of-function features in oncoproteins that arise from recurrent truncating mutations in transcription factors.

Indexed as

AnimalsCCAAT-Enhancer-Binding Protein-alphaGain of Function MutationGene Expression Regulation, NeoplasticHematopoietic Stem CellsHumansLeukemia, Myeloid, AcuteCCAAT-Enhancer-Binding Protein-alphaacute myeloid leukemiaCEBPA (CCAAT/enhancer-binding protein alpha)C/EBPα p30epigenetic landscapetranscription factortruncated isoform

Identifiers

PMID31867767
PMCPMC7115832
OpenAlexW2995560480

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.