ReviewInternational journal of molecular sciences2009
Mitochondrial DNA instability and metabolic shift in human cancers.
Review in International journal of molecular sciences, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 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
67 citing papers in PubMed, 1 synthesis or guideline pooled it, 133 citations in OpenAlex.
- Pooled it
- Pharmacological Potential of Selenoproteins in the Regulation of Oxidative Stress in Liver Diseases.Pharmaceutics · 2026Review
- Bisphenol A disrupts mitochondrial homeostasis and promotes metabolic alterations in cervical cancer cells.Environmental science and pollution research international · 2026Article
- Mitochondrial DNA mutations and intercellular mitochondrial transfer in cancer: mechanisms, biological effects, and clinical potential.Biomarker research · 2026Review
- Mitochondrial DNA Damage and Histological Features in Liver Tissue of Azoxymethane-TreatedBiomolecules · 2025Article
- The Role of Mitochondrial Genome Stability and Metabolic Plasticity in Thyroid Cancer.Biomedicines · 2025Review
- Mitochondrial DNA common deletion in cancer: Emerging evidence and methodological challenges.Computational and structural biotechnology journal · 2025Review
- Mitoepigenetics pathways and natural compounds: a dual approach to combatting hepatocellular carcinoma.Medical oncology (Northwood, London, England) · 2024Review
- Targeting inflammation as cancer therapy.Journal of hematology & oncology · 2024Review
- Impaired Expression of Humanin during Adrenocortical Carcinoma.International journal of molecular sciences · 2024Article
- Unraveling the intricacies of glioblastoma progression and recurrence: insights into the role of NFYB and oxidative phosphorylation at the single-cell level.Frontiers in immunology · 2024Article
- Deciphering the molecular landscape: integrating single-cell transcriptomics to unravel myofibroblast dynamics and therapeutic targets in clear cell renal cell carcinomas.Frontiers in immunology · 2024Article
- Bioenergetic alteration in gastrointestinal cancers: The good, the bad and the ugly.World journal of gastroenterology · 2023Review
- Senataxin and R-loops homeostasis: multifaced implications in carcinogenesis.Cell death discovery · 2023Review
- High leukocyte mitochondrial DNA copy number contributes to poor prognosis in breast cancer patients.BMC cancer · 2023Article
- The Role of Genetic Mutations in Mitochondrial-Driven Cancer Growth in Selected Tumors: Breast and Gynecological Malignancies.Life (Basel, Switzerland) · 2023Review
- Mapping mitonuclear epistasis using a novel recombinant yeast population.PLoS genetics · 2023Article
- Examining the function of macrophage oxidative stress response and immune system in glioblastoma multiforme through analysis of single-cell transcriptomics.Frontiers in immunology · 2023Article
- Article
- Mitochondria as the Essence of Yang Qi in the Human Body.Phenomics (Cham, Switzerland) · 2022Review
7 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
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A shift in glucose metabolism from oxidative phosphorylation to glycolysis is one of the biochemical hallmarks of tumor cells. Mitochondrial defects have been proposed to play an important role in the initiation and/or progression of various types of cancer. In the past decade, a wide spectrum of mutations and depletion of mtDNA have been identified in human cancers. Moreover, it has been demonstrated that activation of oncogenes or mutation of tumor suppressor genes, such as p53, can lead to the upregulation of glycolytic enzymes or inhibition of the biogenesis or assembly of respiratory enzyme complexes such as cytochrome c oxidase. These findings may explain, at least in part, the well documented phenomena of elevated glucose uptake and mitochondrial defects in cancers. In this article, we review the somatic mtDNA alterations with clinicopathological correlations in human cancers, and their potential roles in tumorigenesis, cancer progression, and metastasis. The signaling pathways involved in the shift from aerobic metabolism to glycolysis in human cancers are also discussed.
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.