ReviewiScience2026
Regulatory networks of iron sulfur cluster biology in cancer mechanisms and therapeutic perspectives.
Review in iScience, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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.
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.
Who cites it
3 citing papers in PubMed.
- Cuproptosis and the bioinorganic basis of copper-induced cell death.Journal of biological inorganic chemistry : JBIC : a publication of the Society of Biological Inorganic Chemistry · 2026Review
- Beyond angiogenesis: integrating ferroptosis and metabolic rewiring for next-generation RCC therapy.Frontiers in oncology · 2026Review
- The Methionine-Mitochondria Axis in Cancer: Metabolic Cross-Talk and Therapeutic Vulnerabilities.Current pharmacology reports · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Iron-sulfur (Fe/S) clusters are essential cofactors required for mitochondrial metabolism, redox regulation, DNA synthesis, and cellular viability. Defects in their biogenesis or function compromise mitochondrial homeostasis, iron balance, and genome stability, alterations frequently observed in cancer. Growing evidence indicates that Fe/S proteins participate in tumor cell proliferation, metabolic adaptation, oxidative stress tolerance, and therapeutic resistance. This review summarizes current knowledge on the mechanisms of Fe/S cluster assembly in distinct cellular compartments, including the mitochondria, cytosol, and nucleus, and outlines their physiological roles in normal and malignant cells. It further discusses the molecular mechanisms by which dysregulation of Fe/S cluster homeostasis contributes to tumorigenesis. In addition, we highlight emerging therapeutic strategies that exploit Fe/S cluster dependencies, including small-molecule approaches, regulated cell death pathways, and nanomedicine-based interventions. Collectively, these insights underscore the relevance of Fe/S cluster biology to cancer pathogenesis and its potential for therapeutic exploitation.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.