ReviewCancer communications (London, England)2021
New insights into molecules and pathways of cancer metabolism and therapeutic implications.
Review in Cancer communications (London, England), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers, 2 of them syntheses that pooled it.
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
45 citing papers in PubMed, 2 syntheses or guidelines pooled it.
- Integration of single-cell and bulk RNA-sequencing data reveals the prognostic potential of epithelial gene markers for prostate cancer.Molecular oncology · 2025Pooled it
- Microenvironment immune response induced by tumor ferroptosis-the application of nanomedicine.Frontiers in oncology · 2022Pooled it
- Metabolic rewiring of the tumor microenvironment: therapeutic intervention of multi-pathway adaptations to impede cancer metastasis.Frontiers in molecular biosciences · 2026Review
- Article
- HKDC1 promotes ovarian cancer progression through boosting lipid metabolism and immune escape by stabilizing G6PC/G6PC2.Communications biology · 2025Article
- Ferroptosis: CD8Cell death discovery · 2025Review
- Targeting Ferroptosis: Small-molecule Inducers as Novel Anticancer Agents.Anti-cancer agents in medicinal chemistry · 2025Review
- PCK1 as a target for cancer therapy: from metabolic reprogramming to immune microenvironment remodeling.Cell death discovery · 2024Review
- Role of miRNA‑122 in cancer (Review).International journal of oncology · 2024Review
- Establishment of disulfidptosis-related LncRNA signature as biomarkers in colon adenocarcinoma.Cancer cell international · 2024Article
- The mMolecular cancer · 2024Article
- Computational identification of long non-coding RNAs associated with graphene therapy in glioblastoma multiforme.Brain communications · 2024Article
- The clinical significance of endoplasmic reticulum stress related genes in non-small cell lung cancer and analysis of single nucleotide polymorphism for CAV1.Frontiers in molecular biosciences · 2024Article
- Ferroptosis, autophagy, tumor and immunity.Heliyon · 2023Review
- Small molecule inhibitors for cancer metabolism: promising prospects to be explored.Journal of cancer research and clinical oncology · 2023Review
- MiR-122-5p regulates the mevalonate pathway by targeting p53 in non-small cell lung cancer.Cell death & disease · 2023Article
- Impairment of electron transport chain and induction of apoptosis by chrysin nanoparticles targeting succinate-ubiquinone oxidoreductase in pancreatic and lung cancer cells.Genes & nutrition · 2023Article
- The Role of Reprogrammed Glucose Metabolism in Cancer.Metabolites · 2023Review
- Exploration of Blood Metabolite Signatures of Colorectal Cancer and Polyposis through Integrated Statistical and Network Analysis.Metabolites · 2023Article
- FASN multi-omic characterization reveals metabolic heterogeneity in pancreatic and prostate adenocarcinoma.Journal of translational medicine · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cancer cells are abnormal cells that can reproduce and regenerate rapidly. They are characterized by unlimited proliferation, transformation and migration, and can destroy normal cells. To meet the needs for cell proliferation and migration, tumor cells acquire molecular materials and energy through unusual metabolic pathways as their metabolism is more vigorous than that of normal cells. Multiple carcinogenic signaling pathways eventually converge to regulate three major metabolic pathways in tumor cells, including glucose, lipid, and amino acid metabolism. The distinct metabolic signatures of cancer cells reflect that metabolic changes are indispensable for the genesis and development of tumor cells. In this review, we report the unique metabolic alterations in tumor cells which occur through various signaling axes, and present various modalities available for cancer diagnosis and clinical therapy. We further provide suggestions for the development of anti-tumor therapeutic drugs.
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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.