ReviewCurrent pharmaceutical design2025
A Review Unveiling the Ferroptosis-Regulated Cell Signalling Pathways in Breast Cancer to Elucidate Potent Targets for Cancer Management.
Review in Current pharmaceutical design, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed.
- ARID3A knockdown facilitates ferroptosis partly through modulation of the PTEN/Akt pathway in breast cancer.Oncology letters · 2026Article
- Exploring the synergetic role of cuproptosis and ferroptosis and their implication in advancing cancer therapeutics.Discover oncology · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Recent research suggests that targeting ferroptosis exhibits promise as a potent treatment approach for breast carcinoma. Specific subtypes of tumor cells exhibit heightened vulnerability to ferroptosis-inducing chemicals, which selectively trigger tumor stem cells' demise, enhance tumor cells' sensitivity to chemotherapeutic drugs, and eliminate cancerous cells. Ferroptosis plays a dual role in breast cancer progression, emerging as both a stimulating and inhibitory component. Ferroptosis is effective in treating cancer cells (mesenchymal breast), identified by their ability to undergo Epithelial-mesenchymal Transition (EMT) and their resistance to conventional therapies. Pharmaceutical drugs that hinder the activity of enzymes known as kinases, which are involved in the Akt/mTOR/PI3K signaling pathway, have shown significant potential in the treatment of breast carcinoma. This review investigates the molecular mechanisms of different signaling pathways implicated in ferroptosis in breast carcinoma, with specific emphasis on metastasis, invasion, and proliferation. Our study contributes to understanding a potentially important target that could be used in developing therapeutic strategies for breast cancer treatment.
Indexed as
Identifiers
39901686What 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.