ArticlePLoS genetics2015
Simultaneous DNA and RNA Mapping of Somatic Mitochondrial Mutations across Diverse Human Cancers.
Article in PLoS genetics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 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
79 citing papers in PubMed, 127 citations in OpenAlex.
- TET1-mediated DNA demethylation and transcription activation of MRPS17 induces lung adenocarcinoma through PI3K-AKT-mTOR pathway.Journal of molecular histology · 2026Article
- Comprehensive genome sequencing associates elevated mitochondrial DNA and homoplasmy with early stage I of pancreatic cancer.iScience · 2026Article
- Biological and translational attributes of mitochondrial DNA copy number: Laboratory perspective to clinical relevance.World journal of methodology · 2025Review
- Somatic mtDNA mutations at intermediate levels of heteroplasmy are a source of functional heterogeneity among primary leukemic cells.Science advances · 2025Article
- The Emerging Role of Mitochondrial Dysfunction in Thyroid Cancer: Mediating Tumor Progression, Drug Resistance, and Reshaping of the Immune Microenvironment.Biomolecules · 2025Review
- Glioma grade and mortality in relation to sequence variation in the mitochondrial genome.Cancer genetics · 2025Article
- Exercise, cancer, and the cardiovascular system: clinical effects and mechanistic insights.Basic research in cardiology · 2025Review
- Exploring the oncogenic impact of heteroplasmicMitochondrial communications · 2025Article
- Mitochondrial DNA alterations in precision oncology: Emerging roles in diagnostics and therapeutics.Clinics (Sao Paulo, Brazil) · 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
- Pediatric Chordoma: A Tale of Two Genomes.Molecular cancer research : MCR · 2024Article
- Mitochondrial DNA mosaicism in normal human somatic cells.Nature genetics · 2024Article
- Translatomics to explore dynamic differences in immunocytes in the tumor microenvironment.Molecular therapy. Nucleic acids · 2023Review
- Role of mitochondrial alterations in human cancer progression and cancer immunity.Journal of biomedical science · 2023Review
- Analysis of Mitochondrial Transfer RNA Mutations in Breast Cancer.Balkan journal of medical genetics : BJMG · 2023Article
- mitoSomatic: a tool for accurate identification of mitochondrial DNA somatic mutations without paired controls.Molecular oncology · 2023Article
- Mitochondrial DNA is a major source of driver mutations in cancer.Trends in cancer · 2022Review
- Roles of mitochondrial genetics in cancer metastasis.Trends in cancer · 2022Review
- A method for multiplexed full-length single-molecule sequencing of the human mitochondrial genome.Nature communications · 2022Article
19 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
7 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Somatic mutations in the nuclear genome are required for tumor formation, but the functional consequences of somatic mitochondrial DNA (mtDNA) mutations are less understood. Here we identify somatic mtDNA mutations across 527 tumors and 14 cancer types, using an approach that takes advantage of evidence from both genomic and transcriptomic sequencing. We find that there is selective pressure against deleterious coding mutations, supporting that functional mitochondria are required in tumor cells, and also observe a strong mutational strand bias, compatible with endogenous replication-coupled errors as the major source of mutations. Interestingly, while allelic ratios in general were consistent in RNA compared to DNA, some mutations in tRNAs displayed strong allelic imbalances caused by accumulation of unprocessed tRNA precursors. The effect was explained by altered secondary structure, demonstrating that correct tRNA folding is a major determinant for processing of polycistronic mitochondrial transcripts. Additionally, the data suggest that tRNA clusters are preferably processed in the 3' to 5' direction. Our study gives insights into mtDNA function in cancer and answers questions regarding mitochondrial tRNA biogenesis that are difficult to address in controlled experimental systems.
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.