Evidence map›Paper›PMID 42891769›Full record

ReviewJournal of the Egyptian National Cancer Institute2026

Ferroptosis in cancer: molecular mechanisms, tumour microenvironment, therapeutic resistance, and clinical translation.

Ghisaram Dewasi, Sakshi Jain

Abstract readReview
In one paragraph

Review in Journal of the Egyptian National Cancer Institute, 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

2 authors.

Ghisaram DewasiIndian Council of Medical Research- National Institute of Health Research, Jodhpur, India. Grraika06@gmail.com.ORCID http://orcid.org/0009-0006-5879-7165
Sakshi JainIndian Council of Medical Research- National Institute of Health Research, Jodhpur, India.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ferroptosis is a distinct form of regulated cell death driven by iron-dependent lipid peroxidation and oxidative membrane damage, and it differs fundamentally from apoptosis, necroptosis, and pyroptosis in its molecular mechanisms and execution pathways. Increasing evidence indicates that ferroptosis plays a pivotal role in cancer biology by regulating tumour initiation, progression, metastasis, therapeutic resistance, and interactions within the tumour microenvironment (TME). Dysregulation of iron metabolism, lipid peroxidation, amino acid metabolism, and antioxidant defence systems, including the System Xc⁻-GSH-GPX4, FSP1-CoQ₁₀, GCH1-BH4, and DHODH pathways, collectively determines cellular susceptibility to ferroptosis. Recent studies have further highlighted the contribution of organelle crosstalk, immune cell regulation, and stromal interactions in shaping ferroptotic responses and tumour evolution. In this review, we comprehensively summarise the molecular mechanisms underlying ferroptosis, its regulatory signalling networks, and the major milestones that have advanced the field. We further discuss the multifaceted role of ferroptosis across diverse malignancies, its influence on epithelial-mesenchymal transition, tumour invasion, metastasis, and immune modulation, and its emerging significance in overcoming resistance to chemotherapy, radiotherapy, targeted therapy, and immunotherapy. In addition, we critically evaluate recent progress in ferroptosis-based therapeutic strategies, including nanomedicine, combination therapies, and translational advances, while highlighting current clinical challenges such as tumour heterogeneity, limited pharmacodynamic biomarkers, and safety concerns. Collectively, ferroptosis represents a promising therapeutic vulnerability that bridges fundamental cancer biology with precision oncology. Continued development of biomarker-guided patient stratification, targeted drug delivery systems, and rational combination strategies is expected to accelerate the clinical translation of ferroptosis-based therapies and improve outcomes for patients with refractory and treatment-resistant cancers.

Indexed as

Drug Resistance, NeoplasmFerroptosisNeoplasmsTumor MicroenvironmentAnimalsAntineoplastic AgentsHumansIronSignal TransductionTranslational Research, BiomedicalAntineoplastic AgentsIronCancerClinical translationDrug resistanceFerroptosisImmunotherapyIron metabolismLipid peroxidationNanomedicinePrecision oncologyTumour microenvironment

Identifiers

PMID42891769
PMCPMC13676557

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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.