ReviewGenes & diseases2026
Ferroptosis: The dawn of reversing drug resistance in digestive cancers.
Review in Genes & diseases, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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
6 citing papers in PubMed.
- IntratumorGut microbes · 2026Article
- Pan-cancer analysis identifies KANSL2 as a cell-cycle-associated regulator of tumor progression and immunity in liver hepatocellular carcinoma.Clinical and experimental medicine · 2026Article
- Ferroptosis Resistance: Redundant Antioxidant Networks Are a Barrier to Cancer Therapy.Antioxidants (Basel, Switzerland) · 2026Review
- A clinical decision framework for redox-adapted, EMT-high cancers: From ferroptosis resistance to precision therapeutic stratification.Redox biology · 2026Review
- HDAC inhibitors as ferroptosis sensitizers in cancer: Epigenetic regulation of redox balance and iron metabolism.EXCLI journal · 2026Review
- Harnessing ferroptosis for cancer therapy: Mechanisms and therapeutic strategies (Review).Oncology 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
Ferroptosis, a form of iron-dependent cell death characterized by lipid peroxidation, has emerged as a promising strategy to overcome resistance to chemotherapy. This review explores the mechanisms of ferroptosis and its potential to reverse drug resistance in digestive system cancers. We summarize recent advances in understanding the GPX4-regulated pathway, iron metabolism, and lipid peroxidation as key drivers of ferroptosis. It also highlights the roles of tumor heterogeneity, tumor-stroma interactions, abnormal apoptosis, metabolic alterations, and the tumor microenvironment in drug resistance. Specific mechanisms of ferroptosis resistance in esophageal squamous cell carcinoma, gastric cancer, hepatocellular carcinoma, pancreatic ductal adenocarcinoma, and colorectal cancer are discussed, along with strategies to induce ferroptosis to reverse drug resistance. Future research should focus on translating these findings into clinical applications through targeted therapies and combination treatments to improve patient outcomes.
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What Socratic 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 Socratic graph.