ArticleThe American journal of pathology2002
Mitochondrial DNA somatic mutations (point mutations and large deletions) and mitochondrial DNA variants in human thyroid pathology: a study with emphasis on Hürthle cell tumors.
Article in The American journal of pathology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 106 papers, 2 of them syntheses that pooled it.
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106 citing papers in PubMed, 2 syntheses or guidelines pooled it, 271 citations in OpenAlex.
- Dual-tracerFrontiers in endocrinology · 2025Pooled it
- Pooled it
- Emerging perspectives in proteostasis: bridging mechanisms and therapeutics for human diseases.Signal transduction and targeted therapy · 2026Review
- DNA Damage and Repair in Thyroid Physiology and Disease.Endocrine reviews · 2026Review
- Mitochondria and tumorigenesis: Molecular basis and therapeutic implications.Genes & diseases · 2026Review
- Mitochondrial DNA variations and risk of incident gestational diabetes mellitus: a nested case-control study.Acta diabetologica · 2025Article
- Mutational analysis of the mitochondrial tRNA genes and flanking regions in lymphocytes from long-term pediatric cancer survivors given doxorubicin chemotherapy for acute lymphoblastic leukemia.Cardio-oncology (London, England) · 2025Article
- Article
- 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
- Ultrasound Pattern of Indeterminate Thyroid Nodules with Prevalence of Oncocytes.Journal of clinical medicine · 2025Article
- Article
- Endocrine manifestations and long-term outcomes of patients with mitochondrial diseases.Orphanet journal of rare diseases · 2025Article
- Mitochondrial Complex I Molecular Alterations in Sapajus apella as a Human Gastric Carcinogenesis Model After MNU Exposure.Journal of medical primatology · 2025Article
- Mitochondrial DNA common deletion in cancer: Emerging evidence and methodological challenges.Computational and structural biotechnology journal · 2025Review
- Article
- Identification of sequence polymorphism in the D-loop region of mitochondrial DNA as a risk factor for breast cancer.Cancer science · 2024Article
- Pathogenic mitochondrial DNA mutations inhibit melanoma metastasis.Science advances · 2024Article
- Biomarkers in Thyroid Cancer: Emerging Opportunities from Non-Coding RNAs and Mitochondrial Space.International journal of molecular sciences · 2024Review
- N-Nitrosomorpholine-induced oncocytic transformation in rat endocrine organs.European journal of medical research · 2024Article
46 more citing papers are in PubMed but not listed here.
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In an attempt to progress in the understanding of the relationship of mitochondrial DNA (mtDNA) alterations and thyroid tumorigenesis, we studied the mtDNA in 79 benign and malignant tumors (43 Hürthle and 36 non-Hürthle cell neoplasms) and respective normal parenchyma. The mtDNA common deletion (CD) was evaluated by semiquantitative polymerase chain reaction. Somatic point mutations and sequence variants of mtDNA were searched for in 66 tumors (59 patients) and adjacent parenchyma by direct sequencing of 70% of the mitochondrial genome (including all of the 13 OXPHOS system genes). We detected 57 somatic mutations, mostly transitions, in 34 tumors and 253 sequence variants in 59 patients. Follicular and papillary carcinomas carried a significantly higher prevalence of non-silent point mutations of complex I genes than adenomas. We also detected a significantly higher prevalence of complex I and complex IV sequence variants in the normal parenchyma adjacent to the malignant tumors. Every Hürthle cell tumor displayed a relatively high percentage (up to 16%) of mtDNA CD independently of the lesion's histotype. The percentage of deleted mtDNA molecules was significantly higher in tumors with D-loop mutations than in mtDNA stable tumors. Sequence variants of the ATPase 6 gene, one of the complex V genes thought to play a role in mtDNA maintenance and integrity in yeast, were significantly more prevalent in patients with Hürthle cell tumors than in patients with non-Hürthle cell neoplasms. We conclude that mtDNA variants and mtDNA somatic mutations of complex I and complex IV genes seem to be involved in thyroid tumorigenesis. Germline polymorphisms of the ATPase 6 gene are associated with the occurrence of mtDNA CD, the hallmark of Hürthle cell tumors.
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