ReviewOncogene2006
Mitochondrial DNA mutations in human cancer.
Review in Oncogene, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 280 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
280 citing papers in PubMed, 577 citations in OpenAlex.
- Quantifying circulating cell-free DNA in humans.Scientific reports · 2019Trial
- FOXQ1 promotes endometriosis development by enhancing mitochondrial function.Biological research · 2026Article
- Advances in Elucidating the Mitochondrial DNA Mechanisms Underlying Ozone-Induced Inflammation.Toxics · 2026Review
- Population-specific genomic risk markers for oral and maxillofacial malignancies in a high tobacco-exposure cohort from Eastern Uttar Pradesh, India.Bioinformation · 2026Article
- Mitochondrial metabolic plasticity in cancer: hybrid bioenergetic states and translational targeting in surgical oncology.Experimental biology and medicine (Maywood, N.J.) · 2026Review
- Nanopore detection of single-nucleotide RNA mutations and modifications with programmable nanolatches.Nature nanotechnology · 2025Article
- The Role of Mitochondrial DNA in Modulating Chemoresistance in Esophageal Cancer: Mechanistic Insights and Therapeutic Potential.Biomolecules · 2025Review
- Novel Azole-Modified Porphyrins for Mitochondria-Targeted Photodynamic Therapy.Molecules (Basel, Switzerland) · 2025Article
- Review
- The interplay of mitochondrial dysfunction and altered metabolic pathways in glioblastoma.Contemporary oncology (Poznan, Poland) · 2025Review
- Targeting the epigenome and tumor heterogeneity: advances in immunotherapy for chemoresistant metastatic colorectal cancer.Frontiers in immunology · 2025Review
- The role of mitochondria in tumor metastasis and advances in mitochondria-targeted cancer therapy.Cancer metastasis reviews · 2024Review
- New insights on mitochondrial heteroplasmy observed in ovarian diseases.Journal of advanced research · 2024Review
- Non-Coding RNAs of Mitochondrial Origin: Roles in Cell Division and Implications in Cancer.International journal of molecular sciences · 2024Review
- Simultaneous targeting of peripheral and brain tumors with a therapeutic nanoparticle to disrupt metabolic adaptability at both sites.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Defects of mitochondria-lysosomes communication induce secretion of mitochondria-derived vesicles and drive chemoresistance in ovarian cancer cells.Cell communication and signaling : CCS · 2024Article
- Anticancer Drug Discovery Based on Natural Products: From Computational Approaches to Clinical Studies.Biomedicines · 2024Review
- Article
- Causal relationships between mitochondrial proteins and different pathological types of lung cancer: a bidirectional mendelian randomization study.Frontiers in genetics · 2024Article
- Probing the dynamic crosstalk of lysosomes and mitochondria with structured illumination microscopy.Trends in analytical chemistry : TRAC · 2023Article
220 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 at 2 institutions in 1 country.
Funding
Abstract
Somatic mitochondrial DNA (mtDNA) mutations have been increasingly observed in primary human cancers. As each cell contains many mitochondria with multiple copies of mtDNA, it is possible that wild-type and mutant mtDNA can co-exist in a state called heteroplasmy. During cell division, mitochondria are randomly distributed to daughter cells. Over time, the proportion of the mutant mtDNA within the cell can vary and may drift toward predominantly mutant or wild type to achieve homoplasmy. Thus, the biological impact of a given mutation may vary, depending on the proportion of mutant mtDNAs carried by the cell. This effect contributes to the various phenotypes observed among family members carrying the same pathogenic mtDNA mutation. Most mutations occur in the coding sequences but few result in substantial amino acid changes raising questions as to their biological consequence. Studies reveal that mtDNA play a crucial role in the development of cancer but further work is required to establish the functional significance of specific mitochondrial mutations in cancer and disease progression. The origin of somatic mtDNA mutations in human cancer and their potential diagnostic and therapeutic implications in cancer are discussed. This review article provides a detailed summary of mtDNA mutations that have been reported in various types of cancer. Furthermore, this review offers some perspective as to the origin of these of mutations, their functional consequences in cancer development, and possible therapeutic implications.
Indexed as
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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.