ArticleCancer cell2018
Integrated Genomic Analysis of Hürthle Cell Cancer Reveals Oncogenic Drivers, Recurrent Mitochondrial Mutations, and Unique Chromosomal Landscapes.
Article in Cancer cell, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 143 papers, 2 of them syntheses that pooled it.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
143 citing papers in PubMed, 2 syntheses or guidelines pooled it.
- 2025 American Thyroid Association Management Guidelines for Adult Patients with Differentiated Thyroid Cancer.Thyroid : official journal of the American Thyroid Association · 2025Guideline
- Hürthle Cell Carcinoma of the Thyroid Gland: Systematic Review and Meta-analysis.Advances in therapy · 2021Pooled it
- Molecular Diagnostics and [Thyroid : official journal of the American Thyroid Association · 2024Trial
- Article
- EIF1AX Mutations in thyroid nodules and advanced thyroid carcinoma: a systematic review and meta-analysis.Virchows Archiv : an international journal of pathology · 2026Review
- Molecular Profile of Advanced Radioiodine-refractory Thyroid Cancer and Response to Lenvatinib Treatment.The Journal of clinical endocrinology and metabolism · 2026Article
- Thyroid cancer and double-strand DNA break repair: The potential role of the MRN complex pathogenic variants.Journal of clinical & translational endocrinology · 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
- Genome near-haploidization in CDC73-wildtype parathyroid tumors.Scientific reports · 2026Article
- Review
- Genomic Catastrophe Defines the Evolutionary Trajectory of Adrenocortical Carcinoma.Endocrine pathology · 2026Article
- Integrative transcriptomics and electrophysiological profiling of hiPSC-derived neurons identifies novel druggable pathways in Koolen-de Vries Syndrome.Molecular psychiatry · 2026Article
- Precision medicine in thyroid nodules: current strategies, challenges, and future directions.Hormones (Athens, Greece) · 2026Review
- Mitochondrial DNA mutations and intercellular mitochondrial transfer in cancer: mechanisms, biological effects, and clinical potential.Biomarker research · 2026Review
- Epidemiology and prognostic factors of Hürthle-oncocytic cell carcinoma of the thyroid.Discover oncology · 2026Article
- Review
- 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
- Diagnosing the silent: the molecular landscape of non-functional parathyroid carcinoma.Virchows Archiv : an international journal of pathology · 2025Review
- Article
83 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
23 authors.
Funding
Abstract
The molecular foundations of Hürthle cell carcinoma (HCC) are poorly understood. Here we describe a comprehensive genomic characterization of 56 primary HCC tumors that span the spectrum of tumor behavior. We elucidate the mutational profile and driver mutations and show that these tumors exhibit a wide range of recurrent mutations. Notably, we report a high number of disruptive mutations to both protein-coding and tRNA-encoding regions of the mitochondrial genome. We reveal unique chromosomal landscapes that involve whole-chromosomal duplications of chromosomes 5 and 7 and widespread loss of heterozygosity arising from haploidization and copy-number-neutral uniparental disomy. We also identify fusion genes and disrupted signaling pathways that may drive disease pathogenesis.
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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.