Evidence map›Paper›PMID 31101865›Full record

ReviewNature reviews. Cancer2019

Ferroptosis at the crossroads of cancer-acquired drug resistance and immune evasion.

José Pedro Friedmann Angeli, Dmitri V Krysko, Marcus Conrad

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Cancer, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 743 papers.

0numbers the graph read from it
0cells of the map it votes in
743citing 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

743 citing papers in PubMed.

  1. Review
  2. Article
  3. Ultrasound-activated CuJournal of nanobiotechnology · 2026
    Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. Review
  10. Review
  11. Review
  12. Review
  13. Review
  14. Article
  15. Article
  16. Ferroptosis is a Physiologic Vulnerability of Iron-Recycling Macrophages.bioRxiv : the preprint server for biology · 2026
    Article
  17. Article
  18. Review
  19. Article
  20. Article

683 more citing papers are in PubMed but not listed here.

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.

José Pedro Friedmann AngeliRudolf Virchow Center for Experimental Biomedicine, University of Würzburg, Würzburg, Germany. pedro.angeli@virchow.uni-wuerzburg.de.ORCID http://orcid.org/0000-0001-7706-1379
Dmitri V KryskoDepartment of Human Structure and Repair, Ghent University and Cancer Research Institute Ghent (CRIG), Ghent, Belgium.ORCID http://orcid.org/0000-0002-9692-2047
Marcus ConradInstitute of Developmental Genetics, Helmholtz Zentrum München, Neuherberg, Germany. marcus.conrad@helmholtz-muenchen.de.ORCID http://orcid.org/0000-0003-1140-5612

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ferroptosis is a recently recognized cell death modality that is morphologically, biochemically and genetically distinct from other forms of cell death and that has emerged to play an important role in cancer biology. Recent discoveries have highlighted the metabolic plasticity of cancer cells and have provided intriguing insights into how metabolic rewiring is a critical event for the persistence, dedifferentiation and expansion of cancer cells. In some cases, this metabolic reprogramming has been linked to an acquired sensitivity to ferroptosis, thus opening up new opportunities to treat therapy-insensitive tumours. However, it is not yet clear what metabolic determinants are critical for therapeutic resistance and evasion of immune surveillance. Therefore, a better understanding of the processes that regulate ferroptosis sensitivity should ultimately aid in the discovery of novel therapeutic strategies to improve cancer treatment. In this Perspectives article, we provide an overview of the known mechanisms that regulate sensitivity to ferroptosis in cancer cells and how the modulation of metabolic pathways controlling ferroptosis might reshape the tumour niche, leading to an immunosuppressive microenvironment that promotes tumour growth and progression.

Indexed as

Cell DeathDrug Resistance, NeoplasmHumansNeoplasmsTumor EscapeTumor Microenvironment

Identifiers

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.