Evidence map›Paper›PMID 42278500›Full record

ArticleInternational journal of molecular sciences2026

Wild-Type p53 Protein Enhances APR-246-Induced Cytotoxicity in Acute Myeloid Leukemia and Normal Hematopoietic Stem/Progenitor Cells.

John B Cart, David Zhu, Lucas Norris, Sadhna O Piryani, Li-Chan Chang, Christine E Eyler, Chang-Lung Lee

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in International journal of molecular sciences, 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

7 authors.

John B CartDepartment of Radiation Oncology, Duke University School of Medicine, Durham, NC 27708, USA.
David ZhuDepartment of Radiation Oncology, Duke University School of Medicine, Durham, NC 27708, USA.
Lucas NorrisDepartment of Radiation Oncology, Duke University School of Medicine, Durham, NC 27708, USA.
Sadhna O PiryaniDepartment of Medicine, Duke University School of Medicine, Durham, NC 27708, USA.
Li-Chan ChangDepartment of Radiation Oncology, Duke University School of Medicine, Durham, NC 27708, USA.
Christine E EylerDepartment of Radiation Oncology, Duke University School of Medicine, Durham, NC 27708, USA.
Chang-Lung LeeDepartment of Radiation Oncology, Duke University School of Medicine, Durham, NC 27708, USA.ORCID 0000-0002-0673-633X

Funding

Minimizing the risk of therapy-related myeloid neoplasms by inhibiting genotoxic stress-induced expansion of leukemia-initiating cells with p53 mutationsR03CA249562 · NCI · DUKE UNIVERSITY · PI LEE, CHANG-LUNG · 2021 to 2022
$161k
Duke Medical Center Whitehead Scholar AwardNational Health Institute R03CA249562NCI NIH HHS R03 CA249562
6 · The paper itself

Abstract

APR-246 (Eprenetapopt) is a small-molecule drug that restores the activity of dysfunctional p53 proteins caused by missense mutations that affect the DNA-binding domain. However, recent studies suggest that APR-246 can also induce cell death in cancer cells that carry wild-type (WT)

Indexed as

Hematopoietic Stem CellsLeukemia, Myeloid, AcuteQuinuclidinesTumor Suppressor Protein p53AnimalsApoptosisCell Line, TumorCell SurvivalHumansMiceReactive Oxygen SpecieseprenetapoptQuinuclidinesReactive Oxygen SpeciesTumor Suppressor Protein p53acute myeloid leukemiaAPR-246hematopoietic stem/progenitor cellstumor suppressor TP53

Identifiers

PMID42278500
PMCPMC13257158

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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.