ReviewDiscover oncology2026
Ferroptosis as a novel targeted therapy in gynecological malignant tumors.
Review in Discover oncology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
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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
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Who cites it
0 citing papers in PubMed.
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Authors and funding
12 authors.
Funding
Abstract
Ferroptosis, an emerging form of regulated cell death driven by iron-dependent lipid peroxidation, represents a promising therapeutic target in oncology. Gynecological malignancies—cervical, endometrial, and ovarian cancers—are frequently associated with therapeutic resistance due to defective cell death regulation. This review delineates cancer-specific ferroptosis regulatory networks across these malignancies. In cervical cancer, high-risk HPV oncoproteins (E6/E7) rewire oxidative stress and lipid metabolism, leading to stage-dependent ferroptosis vulnerability and supporting combination approaches with immunotherapy. In endometrial cancer, ELK1-mediated GPX4 upregulation drives chemoresistance, highlighting ferroptosis induction as a strategy to overcome treatment failure. In ovarian cancer, iron overload promotes metastasis, while p53, lipid-modifying enzymes (SCD1/FADS2), and the tumor microenvironment (e.g., CXCL8/CXCR2 axis) modulate ferroptosis sensitivity, providing avenues to target aggressive subtypes such as clear cell carcinoma. We conclude that targeting ferroptosis offers a transformative strategy for gynecological cancers.
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