ReviewJournal of molecular medicine (Berlin, Germany)2011
Inborn and acquired metabolic defects in cancer.
Review in Journal of molecular medicine (Berlin, Germany), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 papers, 1 of them a synthesis 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
84 citing papers in PubMed, 1 synthesis or guideline pooled it.
- The metabolic addiction of cancer stem cells.Frontiers in oncology · 2022Pooled it
- Integrated gene-metabolite association network analysis reveals key metabolic pathways in gastric adenocarcinoma.Heliyon · 2024Article
- Tricarboxylic Acid Cycle Relationships with Non-Metabolic Processes: A Short Story with DNA Repair and Its Consequences on Cancer Therapy Resistance.International journal of molecular sciences · 2024Review
- Fumarate hydratase (FH) and cancer: a paradigm of oncometabolism.British journal of cancer · 2023Review
- Pyruvate transamination and NAD biosynthesis enable proliferation of succinate dehydrogenase-deficient cells by supporting aerobic glycolysis.Cell death & disease · 2023Article
- The connection between tricarboxylic acid cycle enzyme mutations and pseudohypoxic signaling in pheochromocytoma and paraganglioma.Frontiers in endocrinology · 2023Review
- Lack of Major Genome-Wide DNA Methylation Changes in Succinate-Treated Human Epithelial Cells.International journal of molecular sciences · 2022Article
- Review
- Metabostemness in cancer: Linking metaboloepigenetics and mitophagy in remodeling cancer stem cells.Stem cell reviews and reports · 2022Review
- Cancer metabolism: looking forward.Nature reviews. Cancer · 2021Review
- The impact of mitochondria on cancer treatment resistance.Cellular oncology (Dordrecht, Netherlands) · 2021Review
- Review
- Article
- Review
- Redox Potential of Antioxidants in Cancer Progression and Prevention.Antioxidants (Basel, Switzerland) · 2020Review
- Flavonoids against the Warburg phenotype-concepts of predictive, preventive and personalised medicine to cut the Gordian knot of cancer cell metabolism.The EPMA journal · 2020Review
- Oncometabolites and the response to radiotherapy.Radiation oncology (London, England) · 2020Review
- HEREDITARY ENDOCRINE TUMOURS: CURRENT STATE-OF-THE-ART AND RESEARCH OPPORTUNITIES: Metastatic pheochromocytomas and paragangliomas: proceedings of the MEN2019 workshop.Endocrine-related cancer · 2020Review
- Towards the routine use of in silico screenings for drug discovery using metabolic modelling.Biochemical Society transactions · 2020Review
- Oncometabolites in renal cancer.Nature reviews. Nephrology · 2020Review
24 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The observation that altered metabolism is the fundamental cause of cancer was made by Otto Warburg nearly a century ago. However, the subsequent identification of oncogenes and tumor suppressor genes has displaced Warburg's theory pointing towards genetic aberrations as the underlining cause of cancer. Nevertheless, in the last decade, cancer-associated mutations have been identified in genes coding for tricarboxylic acid cycle (TCA cycle, also known as Krebs cycle) and closely related enzymes that have essential roles in cellular metabolism. These observations have revived interest in Warburg's hypothesis and prompted a flurry of functional studies in the hope of gaining mechanistic insight into the links between mitochondrial dysfunction, metabolic alterations, and cancer. In this review, we discuss the potential pro-oncogenic signaling role of some TCA cycle metabolites and their derivatives (oncometabolites). In particular, we focus on their effects on dioxygenases, a family of oxygen and α-ketoglutarate-dependent enzymes that control, among other things, the levels and activity of the hypoxia-inducible transcription factors and the activity of DNA and histone demethylases.
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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.