Evidence map›Paper›PMID 41640441›Full record

ReviewFrontiers in oncology2025

NCOA4 and ferritinophagy in hematological malignancies: a double-edged regulator of iron metabolism and cell fate.

T Chabane, D Bouscary, E Grignano

Abstract readReview
In one paragraph

Review in Frontiers in oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing 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

6 citing papers in PubMed.

  1. Review
  2. Article
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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

3 authors.

T ChabaneUniversité de Paris, Institut Cochin, CNRS UMR 8104, INSERM U1016, Paris, France.
D BouscaryUniversité de Paris, Institut Cochin, CNRS UMR 8104, INSERM U1016, Paris, France.
E GrignanoDivision of Hematology, Department of Medicine, McGill University, Montreal, QC, Canada.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ferritinophagy, a selective autophagic process mediated by NCOA4, plays a central role in cellular iron homeostasis by mobilizing iron from ferritin to sustain mitochondrial metabolism and redox balance. In cancer, ferritinophagy's effects vary with context: it can support metabolic fitness in some settings while promoting ferroptotic vulnerability in others. In acute myeloid leukemia (AML), evidence suggests that leukemic stem cells rely more heavily on iron-driven mitochondrial metabolism, making ferritinophagy a potential therapeutic target. This review summarizes current knowledge of NCOA4 regulation and ferritinophagy, discusses their relevance in hematologic malignancies, and highlights therapeutic opportunities and unresolved questions in AML.

Indexed as

acute myeloid leukemiaCHIPferritinophagyferroptosisironNCOA4reactive oxygen speciesTet2

Identifiers

PMID41640441
PMCPMC12864102

What OpenQuestion 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 OpenQuestion graph.