ReviewJournal of ovarian research2026
Ferroptosis and chemotherapy resistance in ovarian cancer: molecular mechanisms and therapeutic opportunities.
Review in Journal of ovarian research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. 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.
- Correction: Ferroptosis and chemotherapy resistance in ovarian cancer: molecular mechanisms and therapeutic opportunities.Journal of ovarian research · 2026Article
- Beyond Junk DNA: Emerging Roles of Non-Coding RNAs in Cancer and Therapeutic Innovation.Biomolecules · 2026Review
- GPX4 in the Tumor Microenvironment: Not Just Inhibiting Ferroptosis, but Immuno-Metabolic Regulation.Biomolecules · 2026Review
Corrections and comments
- Erratum issued
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ovarian cancer remains the most lethal gynecologic malignancy, with acquired platinum resistance accounting for the majority of treatment failures. Ferroptosis, an iron-dependent form of regulated cell death driven by lipid peroxidation, has emerged as a metabolic vulnerability that therapy-resistant cancers cannot fully evade. This review examines the relationship between ferroptosis and chemotherapy resistance in high-grade serous ovarian cancer (HGSOC), analyzing the GPX4 antioxidant axis, polyunsaturated fatty acid biosynthesis, and iron homeostasis. We highlight recent discoveries including BRCA1-dependent ubiquitination of GPX4 and its implications for PARP inhibitor synthetic lethality, NR1D2-mediated transcriptional repression of FSP1, and stromal protection conferred by cancer-associated fibroblasts. The unique features of ovarian cancer-iron-abundant ascites, the lipid-rich omental niche, and prevalent BRCA mutations-present distinctive therapeutic opportunities. We introduce the novel concepts of a "ferroptosis compensatory threshold" requiring concurrent multi-node inhibition, and the need for personalized therapeutic design based on tumor ferroptosis defense profiling. We also address challenges confronting clinical translation: on-target toxicities, resistance mechanisms, spatial heterogeneity in ferroptosis susceptibility, and the need for validated predictive biomarkers. By synthesizing these cutting-edge findings, we provide a framework that integrates cancer genetics, microenvironment metabolism, and immunology, distinguishing this review from previous summaries and highlighting actionable vulnerabilities for overcoming chemoresistance in ovarian cancer.
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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.