ReviewGenes & cancer2018
Tumor metabolism regulating chemosensitivity in ovarian cancer.
Review in Genes & cancer, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 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
40 citing papers in PubMed, 65 citations in OpenAlex.
- Overcoming Therapy Resistance in Ovarian Cancer: From Molecular Mechanisms to Emerging Therapeutic Strategies.Cancers · 2026Review
- The role of circadian disruption, sleep dysregulation, lifestyle factors, and metabolic reprogramming in the pathogenesis and progression of ovarian cancer.Journal of the National Cancer Center · 2026Review
- Promising Role of PKM2 in the Diagnosis and Prognosis of Ovarian Cancer.Anti-cancer agents in medicinal chemistry · 2026Review
- Mechanical cues rewire lipid metabolism and support chemoresistance in epithelial ovarian cancer cell lines OVCAR3 and SKOV3.Cell communication and signaling : CCS · 2025Article
- STK32C modulates doxorubicin resistance in triple-negative breast cancer cells via glycolysis regulation.Molecular and cellular biochemistry · 2025Article
- Phosphorylation of FOXK2 at Thr13 and Ser30 by PDK2 sustains glycolysis through a positive feedback manner in ovarian cancer.Oncogene · 2024Article
- RETRACTED: High PGC-1α Expression as a Poor Prognostic Indicator in Intracranial Glioma.Biomedicines · 2024Article
- Tumor metabolism rewiring in epithelial ovarian cancer.Journal of ovarian research · 2023Review
- Revving the engine: PKB/AKT as a key regulator of cellular glucose metabolism.Frontiers in physiology · 2023Review
- Article
- p53 Modulates Radiosensitivity in Head and Neck Cancers-From Classic to Future Horizons.Diagnostics (Basel, Switzerland) · 2022Review
- Review
- Recent advances in understanding the metabolic plasticity of ovarian cancer: A systematic review.Heliyon · 2022Article
- TMEM14A aggravates the progression of human ovarian cancer cells by enhancing the activity of glycolysis.Experimental and therapeutic medicine · 2022Article
- Targeting mitochondrial metabolism for metastatic cancer therapy.Molecular carcinogenesis · 2022Review
- Platinum-induced mitochondrial OXPHOS contributes to cancer stem cell enrichment in ovarian cancer.Journal of translational medicine · 2022Article
- Metabolic risk factors of ovarian cancer: a review.JBRA assisted reproduction · 2022Review
- Metabolic Alterations and WNT Signaling Impact Immune Response in HGSOC.Clinical cancer research : an official journal of the American Association for Cancer Research · 2022Article
- Understanding the Correlation between Metabolic Regulator SIRT1 and Exosomes with CA-125 in Ovarian Cancer: A Clinicopathological Study.BioMed research international · 2022Article
- Immune-and Metabolism-Associated Molecular Classification of Ovarian Cancer.Frontiers in oncology · 2022Article
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 at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Elevated metabolism is a key hallmark of multiple cancers, serving to fulfill high anabolic demands. Ovarian cancer (OVCA) is the fifth leading cause of cancer deaths in women with a high mortality rate (45%). Chemoresistance is a major hurdle for OVCA treatment. Although substantial evidence suggests that metabolic reprogramming contributes to anti-apoptosis and the metastasis of multiple cancers, the link between tumor metabolism and chemoresistance in OVCA remains unknown. While clinical trials targeting metabolic reprogramming alone have been met with limited success, the synergistic effect of inhibiting tumor-specific metabolism with traditional chemotherapy warrants further examination, particularly in OVCA. This review summarizes the role of key glycolytic enzymes and other metabolic synthesis pathways in the progression of cancer and chemoresistance in OVCA. Within this context, mitochondrial dynamics (fission, fusion and cristae structure) are addressed regarding their roles in controlling metabolism and apoptosis, closely associated with chemosensitivity. The roles of multiple key oncogenes (Akt, HIF-1α) and tumor suppressors (p53, PTEN) in metabolic regulation are also described. Next, this review summarizes recent research of metabolism and future direction. Finally, we examine clinical drugs and inhibitors to target glycolytic metabolism, as well as the rationale for such strategies as potential therapeutics to overcome chemoresistant OVCA.
Indexed as
Identifiers
What 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.