ArticleCancer research2015
Mitochondrial Genetics Regulate Breast Cancer Tumorigenicity and Metastatic Potential.
Article in Cancer research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.
What it found
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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.
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Who cites it
52 citing papers in PubMed, 69 citations in OpenAlex.
- Mitochondrial tRNA-Derived Fragments as Candidate Metastasis-Modifying RNA.Cancer research communications · 2026Article
- Mitophagy's impacts on cancer and neurodegenerative diseases: implications for future therapies.Journal of hematology & oncology · 2025Review
- ER-mitochondria tethering and its signaling: A novel therapeutic target in breast cancer.Molecular therapy. Oncology · 2025Review
- Mitochondrial DNA lineages determine tumor progression through T cell reactive oxygen signaling.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Preclinical models of mitochondrial dysfunction: mtDNA and nuclear-encoded regulators in diverse pathologies.Frontiers in aging · 2025Review
- Mitochondrial DNA alterations in precision oncology: Emerging roles in diagnostics and therapeutics.Clinics (Sao Paulo, Brazil) · 2025Review
- Inter- and intracellular mitochondrial communication: signaling hubs in aging and age-related diseases.Cellular & molecular biology letters · 2024Review
- Shikonin blocks CAF-induced TNBC metastasis by suppressing mitochondrial biogenesis through GSK-3β/NEDD4-1 mediated phosphorylation-dependent degradation of PGC-1α.Journal of experimental & clinical cancer research : CR · 2024Article
- Anti-Cancer Potency of Copper-Doped Carbon Quantum Dots Against Breast Cancer Progression.International journal of nanomedicine · 2024Article
- A Method for Real-Time Assessment of Mitochondrial Respiration Using Murine Corneal Biopsy.Investigative ophthalmology & visual science · 2023Article
- Generating Mitochondrial-Nuclear Exchange (MNX) Mice to Identify Mitochondrial Determinants of Cancer Metastasis.Methods in molecular biology (Clifton, N.J.) · 2023Article
- Roles of mitochondrial genetics in cancer metastasis.Trends in cancer · 2022Review
- Mechanisms of breast cancer metastasis.Clinical & experimental metastasis · 2022Review
- Mitochondria dysfunction in circulating tumor cells.Frontiers in oncology · 2022Review
- Mitochondria and Their Relationship with Common Genetic Abnormalities in Hematologic Malignancies.Life (Basel, Switzerland) · 2021Review
- Mito-Mendelian interactions alter in vivo glucose metabolism and insulin sensitivity in healthy mice.American journal of physiology. Endocrinology and metabolism · 2021Article
- University of Alabama at Birmingham Nathan Shock Center: comparative energetics of aging.GeroScience · 2021Review
- Impact of an MT-RNR1 Gene Polymorphism on Hepatocellular Carcinoma Progression and Clinical Characteristics.International journal of molecular sciences · 2021Article
- Mitochondrial metabolism and DNA methylation: a review of the interaction between two genomes.Clinical epigenetics · 2020Review
- Decoding the rosetta stone of mitonuclear communication.Pharmacological research · 2020Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Current paradigms of carcinogenic risk suggest that genetic, hormonal, and environmental factors influence an individual's predilection for developing metastatic breast cancer. Investigations of tumor latency and metastasis in mice have illustrated differences between inbred strains, but the possibility that mitochondrial genetic inheritance may contribute to such differences in vivo has not been directly tested. In this study, we tested this hypothesis in mitochondrial-nuclear exchange mice we generated, where cohorts shared identical nuclear backgrounds but different mtDNA genomes on the background of the PyMT transgenic mouse model of spontaneous mammary carcinoma. In this setting, we found that primary tumor latency and metastasis segregated with mtDNA, suggesting that mtDNA influences disease progression to a far greater extent than previously appreciated. Our findings prompt further investigation into metabolic differences controlled by mitochondrial process as a basis for understanding tumor development and metastasis in individual subjects. Importantly, differences in mitochondrial DNA are sufficient to fundamentally alter disease course in the PyMT mouse mammary tumor model, suggesting that functional metabolic differences direct early tumor growth and metastatic efficiency.
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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.