ArticleBMC cancer2015
A mutation screening of oncogenes, tumor suppressor gene TP53 and nuclear encoded mitochondrial complex I genes in oncocytic thyroid tumors.
Article in BMC cancer, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 39 citations in OpenAlex.
- Mitochondrial complex I in focus: mechanisms and therapeutic strategies of urinary system diseases.Frontiers in physiology · 2026Review
- Recent advances in mitochondria-targeting theranostic agents.Exploration (Beijing, China) · 2024Review
- Molecular pathology of endocrine gland tumors: genetic alterations and clinicopathologic relevance.Virchows Archiv : an international journal of pathology · 2024Review
- Article
- Genetics, Diagnosis, and Management of Hürthle Cell Thyroid Neoplasms.Frontiers in endocrinology · 2021Review
- Multifaceted Roles of Mitochondrial Components and Metabolites in Metabolic Diseases and Cancer.International journal of molecular sciences · 2020Review
- Multi-omics Signatures and Translational Potential to Improve Thyroid Cancer Patient Outcome.Cancers · 2019Review
- Exome-Wide Rare Variant Analysis From the DiscovEHR Study Identifies Novel Candidate Predisposition Genes for Endometrial Cancer.Frontiers in oncology · 2019Article
- Clinically Relevant Prognostic Parameters in Differentiated Thyroid Carcinoma.Endocrine pathology · 2018Review
- Widespread Chromosomal Losses and Mitochondrial DNA Alterations as Genetic Drivers in Hürthle Cell Carcinoma.Cancer cell · 2018Article
- Potential Use of 1-25-dihydroxyvitamin D in the Diagnosis and Treatment of Papillary Thyroid Cancer.Medical science monitor : international medical journal of experimental and clinical research · 2018Article
- Molecular analysis driven video-assisted thoracic surgery resections in bilateral synchronous lung cancers: from the test tube to the operatory room.Annals of translational medicine · 2017Review
- The General Expression Analysis of WTX Gene in Normal and Cancer Tissues.Pathology oncology research : POR · 2017Article
- The Mitochondrial Complex(I)ty of Cancer.Frontiers in oncology · 2017Review
- Relationship Between P15 Gene Mutation and Formation and Metastasis of Malignant Osteosarcoma.Medical science monitor : international medical journal of experimental and clinical research · 2016Article
- Decoding Warburg's hypothesis: tumor-related mutations in the mitochondrial respiratory chain.Oncotarget · 2015Review
- Oncocytic lesions of the ocular adnexa: A review of the histopathology with a brief discussion of the pathogenesis.Saudi journal of ophthalmology : official journal of the Saudi Ophthalmological SocietyArticle
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Authors and funding
12 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThyroid neoplasias with oncocytic features represent a specific phenotype in non-medullary thyroid cancer, reflecting the unique biological phenomenon of mitochondrial hyperplasia in the cytoplasm. Oncocytic thyroid cells are characterized by a prominent eosinophilia (or oxyphilia) caused by mitochondrial abundance. Although disruptive mutations in the mitochondrial DNA (mtDNA) are the most significant hallmark of such tumors, oncocytomas may be envisioned as heterogeneous neoplasms, characterized by multiple nuclear and mitochondrial gene lesions. We investigated the nuclear mutational profile of oncocytic tumors to pinpoint the mutations that may trigger the early oncogenic hit.
methodsTotal DNA was extracted from paraffin-embedded tissues from 45 biopsies of oncocytic tumors. High-resolution melting was used for mutation screening of mitochondrial complex I subunits genes. Specific nuclear rearrangements were investigated by RT-PCR (RET/PTC) or on isolated nuclei by interphase FISH (PAX8/PPARγ). Recurrent point mutations were analyzed by direct sequencing.
resultsIn our oncocytic tumor samples, we identified rare TP53 mutations. The series of analyzed cases did not include poorly- or undifferentiated thyroid carcinomas, and none of the TP53 mutated cases had significant mitotic activity or high-grade features. Thus, the presence of disruptive TP53 mutations was completely unexpected. In addition, novel mutations in nuclear-encoded complex I genes were identified.
conclusionsThese findings suggest that nuclear genetic lesions altering the bioenergetics competence of thyroid cells may give rise to an aberrant mitochondria-centered compensatory mechanism and ultimately to the oncocytic phenotype.
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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.