Evidence map›Paper›PMID 41512877›Full record

ArticleCell reports. Medicine2026

ΔNp73 isoform defines a TP53-mutant-like poor-risk subgroup of acute myeloid leukemia.

Diego A Pereira-Martins, Cesar Ortiz, Isabel Weinhäuser, Albertus T J Wierenga, Vincent van den Boom, Fatemeh Mojallali, Dominique Sternadt, Nisha K van der Meer, Shanna M Hogeling, Thiago M Bianco and 8 more

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In one paragraph

Article in Cell reports. Medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

18 authors.

Diego A Pereira-MartinsDepartment of Hematology, University Medical Center Groningen, University of Groningen, Groningen, the Netherlands; Department of Medical Imaging, Haematology, and Oncology, Ribeirão Preto Medical School, University of São Paulo, Ribeirão Preto, SP, Brazil; Center for Cell Based Therapy, São Paulo Research Foundation, Ribeirão Preto, SP, Brazil; Hematology Division, LIM31, Faculdade de Medicina, University of São Paulo, São Paulo, Brazil.
Cesar OrtizDepartment of Medical Imaging, Haematology, and Oncology, Ribeirão Preto Medical School, University of São Paulo, Ribeirão Preto, SP, Brazil; Center for Cell Based Therapy, São Paulo Research Foundation, Ribeirão Preto, SP, Brazil; Hematology Division, LIM31, Faculdade de Medicina, University of São Paulo, São Paulo, Brazil.
Isabel WeinhäuserDepartment of Hematology, University Medical Center Groningen, University of Groningen, Groningen, the Netherlands; Department of Medical Imaging, Haematology, and Oncology, Ribeirão Preto Medical School, University of São Paulo, Ribeirão Preto, SP, Brazil; Center for Cell Based Therapy, São Paulo Research Foundation, Ribeirão Preto, SP, Brazil.
Albertus T J WierengaDepartment of Hematology, University Medical Center Groningen, University of Groningen, Groningen, the Netherlands.
Vincent van den BoomDepartment of Hematology, University Medical Center Groningen, University of Groningen, Groningen, the Netherlands.
Fatemeh MojallaliDepartment of Hematology, University Medical Center Groningen, University of Groningen, Groningen, the Netherlands.
Dominique SternadtDepartment of Hematology, University Medical Center Groningen, University of Groningen, Groningen, the Netherlands.
Nisha K van der MeerDepartment of Hematology, University Medical Center Groningen, University of Groningen, Groningen, the Netherlands.
Shanna M HogelingDepartment of Hematology, University Medical Center Groningen, University of Groningen, Groningen, the Netherlands.
Thiago M BiancoDepartment of Medical Imaging, Haematology, and Oncology, Ribeirão Preto Medical School, University of São Paulo, Ribeirão Preto, SP, Brazil; Center for Cell Based Therapy, São Paulo Research Foundation, Ribeirão Preto, SP, Brazil.
Prodromos ChatzikyriakouMyeloid Leukaemia Genomics and Biology Group, School of Cancer and Pharmaceutical Sciences, King's College London, London, UK.
Douglas R SilveiraMyeloid Leukaemia Genomics and Biology Group, School of Cancer and Pharmaceutical Sciences, King's College London, London, UK.
Emanuele AmmatunaDepartment of Hematology, University Medical Center Groningen, University of Groningen, Groningen, the Netherlands.
Antonio R Lucena-AraujoDepartment of Genetics, Federal University of Pernambuco, Recife, Brazil.
Lynn QuekMyeloid Leukaemia Genomics and Biology Group, School of Cancer and Pharmaceutical Sciences, King's College London, London, UK.
Gerwin HulsDepartment of Hematology, University Medical Center Groningen, University of Groningen, Groningen, the Netherlands.
Eduardo M RegoDepartment of Medical Imaging, Haematology, and Oncology, Ribeirão Preto Medical School, University of São Paulo, Ribeirão Preto, SP, Brazil; Center for Cell Based Therapy, São Paulo Research Foundation, Ribeirão Preto, SP, Brazil; Hematology Division, LIM31, Faculdade de Medicina, University of São Paulo, São Paulo, Brazil.
Jan Jacob SchuringaDepartment of Hematology, University Medical Center Groningen, University of Groningen, Groningen, the Netherlands. Electronic address: j.j.schuringa@umcg.nl.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Among acute myeloid leukemia (AML) patients, a subgroup remains notoriously refractory to current treatment options, with underlying mechanisms poorly understood. Here, using a multi-omics approach, we reveal that this resistant patient subgroup is characterized by high expression of the oncogenic TP73 isoform ΔNp73, exhibiting similarly poor outcomes as TP53-mutant AML. ΔNp73, which lacks a transcriptional activation domain but retains chromatin-binding properties, competes with TP53 for specific gene targets, thereby downregulating TP53 signaling. We demonstrate that the transcription factor CEBPA controls ΔNp73 expression in AML cells by binding to an intragenic enhancer region. Genetic or pharmacological inhibition of the transcriptional activity of CEBPA with guanfacine reduces ΔNp73 levels and restores drug sensitivity involving ferroptosis-mediated cell death, acting synergistically with venetoclax. Our study sheds light on a previously undercharacterized poor-risk subgroup of AML, which may support patient stratification and inform treatment considerations.

Indexed as

Leukemia, Myeloid, AcuteMutationTumor Protein p73Tumor Suppressor Protein p53Bridged Bicyclo Compounds, HeterocyclicCCAAT-Enhancer-Binding ProteinsCell Line, TumorDrug Resistance, NeoplasmGene Expression Regulation, LeukemicHumansProtein IsoformsSulfonamidesBridged Bicyclo Compounds, HeterocyclicCCAAT-Enhancer-Binding ProteinsCEBPA protein, humanProtein IsoformsSulfonamidesTP53 protein, humanTP73 protein, humanTumor Protein p73Tumor Suppressor Protein p53venetoclaxacute myeloid leukemiaAML PDX modelsCEBPAdrug resistanceferroptosisguanfacinepoor prognosis predictionSREBP/SREBFTP53-mutated AMLTP73

Identifiers

PMID41512877
PMCPMC12866144

What Socratic 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 Socratic graph.