ArticleProceedings of the National Academy of Sciences of the United States of America2007
Disruptive mitochondrial DNA mutations in complex I subunits are markers of oncocytic phenotype in thyroid tumors.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 127 papers, 1 of them a synthesis that pooled it.
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Who cites it
127 citing papers in PubMed, 1 synthesis or guideline pooled it, 317 citations in OpenAlex.
- Dual-tracerFrontiers in endocrinology · 2025Pooled it
- Oxidative Phosphorylation System in Gastric Carcinomas and Gastritis.Oxidative medicine and cellular longevity · 2017Trial
- Follicular-Patterned Lesions of the Thyroid Gland.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2026Review
- Loss of heterozygosity exposes germline mutations in complex I and drives Warburg metabolism in oncocytic carcinoma of the thyroid.Science advances · 2026Article
- Distinct ALK Expression Patterns Are Associated with Canonical and Noncanonical STRN::ALK Transcript Architectures in Oncocytic Thyroid Neoplasms.Endocrine pathology · 2026Article
- Impact of mitochondrial reductive stress due to respiratory chain limitation on cancer via posttranslational modifications.Redox biology · 2026Review
- Article
- Mitochondrial complex I in focus: mechanisms and therapeutic strategies of urinary system diseases.Frontiers in physiology · 2026Review
- Loss of heterozygosity exposes germline mutations in complex I and drives Warburg metabolism in oncocytic carcinoma of the thyroid.bioRxiv : the preprint server for biology · 2025Article
- New Method Enhanced Extraction of Protein Signatures of Renal Cell Carcinoma from Proteomics Data.Journal of proteome research · 2025Article
- Review
- The Role of Mitochondrial Genome Stability and Metabolic Plasticity in Thyroid Cancer.Biomedicines · 2025Review
- Somatic genetic alterations in the development and progression in thyroid tumors of follicular cells.European thyroid journal · 2025Review
- Histopathological, Immunohistochemical, Molecular and Genetic Biomarkers in Differentiated Thyroid Cancer.Cancers · 2025Review
- Circulating Biomarkers of Thyroid Cancer: An Appraisal.Journal of clinical medicine · 2025Review
- Various genetic alterations observed in both benign and malignant oncocytic (Hürthle cell) neoplasms of the thyroid.CytoJournal · 2025Article
- Biomarkers in Thyroid Cancer: Emerging Opportunities from Non-Coding RNAs and Mitochondrial Space.International journal of molecular sciences · 2024Review
- Forward Genetic Screens Identify Mechanisms of Resistance to Small-Molecule Lactate Dehydrogenase Inhibitors.ACS chemical biology · 2024Article
- Molecular pathology of endocrine gland tumors: genetic alterations and clinicopathologic relevance.Virchows Archiv : an international journal of pathology · 2024Review
- Oncocytic Carcinoma with Liver Metastasis: Unusual Treatment Strategies and Clinical Insights-A Case Report and Review of the Literature.Case reports in oncological medicine · 2024Article
67 more citing papers are in PubMed but not listed here.
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Authors and funding
16 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Oncocytic tumors are a distinctive class of proliferative lesions composed of cells with a striking degree of mitochondrial hyperplasia that are particularly frequent in the thyroid gland. To understand whether specific mitochondrial DNA (mtDNA) mutations are associated with the accumulation of mitochondria, we sequenced the entire mtDNA in 50 oncocytic lesions (45 thyroid tumors of epithelial cell derivation and 5 mitochondrion-rich breast tumors) and 52 control cases (21 nononcocytic thyroid tumors, 15 breast carcinomas, and 16 gliomas) by using recently developed technology that allows specific and reliable amplification of the whole mtDNA with quick mutation scanning. Thirteen oncocytic lesions (26%) presented disruptive mutations (nonsense or frameshift), whereas only two samples (3.8%) presented such mutations in the nononcocytic control group. In one case with multiple thyroid nodules analyzed separately, a disruptive mutation was found in the only nodule with oncocytic features. In one of the five mitochondrion-rich breast tumors, a disruptive mutation was identified. All disruptive mutations were found in complex I subunit genes, and the association between these mutations and the oncocytic phenotype was statistically significant (P=0.001). To study the pathogenicity of these mitochondrial mutations, primary cultures from oncocytic tumors and corresponding normal tissues were established. Electron microscopy and biochemical and molecular analyses showed that primary cultures derived from tumors bearing disruptive mutations failed to maintain the mutations and the oncocytic phenotype. We conclude that disruptive mutations in complex I subunits are markers of thyroid oncocytic tumors.
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