ReviewJournal of advanced research2026
Metabolic vulnerabilities in ovarian cancer decoding the nexus between nutrient adaptation and therapy resistance.
Review in Journal of advanced research, 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
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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
6 citing papers in PubMed.
- Subtype-specific mechanisms of lipid metabolism in gynecological malignancies and novel targeted intervention strategies (Review).Oncology letters · 2026Review
- Overcoming Therapy Resistance in Ovarian Cancer: From Molecular Mechanisms to Emerging Therapeutic Strategies.Cancers · 2026Review
- Liquid Biopsy-Based Metabolomics in Epithelial Ovarian Cancer: Challenges, Methodological Advances and Translational Considerations.Diagnostics (Basel, Switzerland) · 2026Review
- Machine learning-based identification of an oxidative phosphorylation signature for prognosis, immune infiltration, and drug sensitivity in ovarian cancer.Frontiers in immunology · 2026Article
- The enigmatic role of tumor dormancy cells in gynecologic cancers.Frontiers in immunology · 2026Review
- Deciphering mitochondrial metabolic vulnerabilities in ovarian clear cell carcinoma with mass spectrometry-based clinical proteomics.Expert review of proteomicsReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundOvarian cancer (OC) is a leading cause of gynecologic cancer-related mortality, primarily due to frequent therapy resistance and disease recurrence. Growing evidence indicates that metabolic reprogramming serves as a critical adaptive mechanism, allowing cancer cells to survive therapeutic stress. AIM OF REVIEW: This review aims to decode the interplay between nutrient adaptation and therapy resistance in OC. It examines how alterations in key metabolic pathways contribute to treatment resilience and disease progression, and explores the potential of targeting metabolic vulnerabilities to improve therapeutic outcomes. KEY SCIENTIFIC CONCEPTS OF REVIEW: We discuss how OC cells utilize metabolic pathways-including glycolysis, OXPHOS, glutamine metabolism, and lipid utilization-to promote survival, DNA repair, and immune evasion. Metabolic plasticity enables shifts between nutrient sources, driving resistance to platinum-based agents, PARP inhibitors, and anti-angiogenic therapies. These adaptations vary across subtypes, such as high-grade serous and clear cell carcinomas, and are influenced by specific mutations. Targeting metabolic enzymes-such as GLS, CPT1, OXPHOS complexes, or NAD
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Registered trials
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