ArticleAnnals of medicine and surgery (2012)2026
Disulfidptosis: The metabolic Achilles' heel of SLC7A11-high tumors and why oncology has missed it.
Article in Annals of medicine and surgery (2012), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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
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.
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Who cites it
1 citing paper in PubMed.
- Glucose Transporters: Structure, Trafficking, Physiology, and Disease Relevance.Current issues in molecular biology · 2026Review
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
SLC7A11 overexpression is one of the most consistent features of treatment-resistant solid tumors, yet its metabolic liabilities remain therapeutically unexploited. Tumors that upregulate SLC7A11 import large quantities of cystine to fuel glutathione synthesis and resist ferroptosis, a strategy that renders them addicted to glucose-derived NADPH for disulfide reduction. Under glucose limitation, NADPH depletion causes toxic cystine accumulation, aberrant disulfide bonding of actin cytoskeletal proteins, F-actin collapse, and a distinct form of regulated cell death termed disulfidptosis. First characterized in 2023, disulfidptosis operates independently of caspases, lipid peroxidation, and reactive oxygen species, and cannot be rescued by inhibitors of apoptosis, ferroptosis, or necroptosis. Recent evidence shows that this pathway extends beyond cancer cells: intratumoral CD8+ T cells undergo SLC7A11-dependent disulfidptosis, contributing to T cell exhaustion and immune evasion. Glucose transporter inhibitors such as BAY-876 selectively trigger disulfidptosis in SLC7A11-high patient-derived xenografts while sparing SLC7A11-low tumors. Despite this, no clinical oncology framework currently stratifies patients by SLC7A11-dependent metabolic vulnerability, and no disulfidptosis-targeting agent has entered clinical trials. Challenges include the absence of validated
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