ArticleEndocrine-related cancer2012
Thyroid-specific ablation of the Carney complex gene, PRKAR1A, results in hyperthyroidism and follicular thyroid cancer.
Article in Endocrine-related cancer, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.
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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
30 citing papers in PubMed, 1 synthesis or guideline pooled it, 38 citations in OpenAlex.
- Association between subclinical hyperthyroidism and aFrontiers in endocrinology · 2022Pooled it
- Multifaceted roles of superoxide dismutases (SODs) in cellular homeostasis and cancer progression: Redox regulation and therapeutic implications.Journal of medical biochemistry · 2026Article
- A case series and literature review of thyroid cancer presenting with thyroid hot nodule.SAGE open medical case reports · 2026Article
- In vivo and in vitro analysis of functional effects of the SDHD H50R variant.Endocrine-related cancer · 2025Article
- Hyperthyroidism Due to Functioning Metastatic Bone Lesions of Follicular Thyroid Carcinoma Treated With Lenvatinib.JCEM case reports · 2024Article
- A Rare Case of Functional Metastatic Follicular Thyroid Carcinoma With Concomitant Thyrotoxicosis.Case reports in endocrinology · 2024Article
- Carney Complex and Its Association With Thyroid Cancer, Molecular Pathway, and Treatment.Cureus · 2023Review
- Pathogenesis of cancers derived from thyroid follicular cells.Nature reviews. Cancer · 2023Review
- Cancer Predisposition Syndromes and Thyroid Cancer: Keys for a Short Two-Way Street.Biomedicines · 2023Review
- Mouse Models to Examine Differentiated Thyroid Cancer Pathogenesis: Recent Updates.International journal of molecular sciences · 2023Review
- Case Report: Atrial myxoma combined with hyperthyroidism in an adolescent with literature review.Frontiers in oncology · 2023Article
- Preclinical Models of Neuroendocrine Neoplasia.Cancers · 2022Review
- Review
- Sex Bias in Differentiated Thyroid Cancer.International journal of molecular sciences · 2021Review
- Review
- Genetic Mutations and Variants in the Susceptibility of Familial Non-Medullary Thyroid Cancer.Genes · 2020Review
- Hyperfunctioning thyroid carcinoma: A systematic review.Molecular and clinical oncology · 2019Article
- PKA Activates AMPK Through LKB1 Signaling in Follicular Thyroid Cancer.Frontiers in endocrinology · 2019Article
- Alterations in Sod2-Induced Oxidative Stress Affect Endocrine Cancer Progression.The Journal of clinical endocrinology and metabolism · 2018Article
- Deletion of Rap1b, but not Rap1a or Epac1, Reduces Protein Kinase A-Mediated Thyroid Cancer.Thyroid : official journal of the American Thyroid Association · 2018Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Thyroid cancer is the most common endocrine malignancy in the population, and the incidence of this cancer is increasing at a rapid rate. Although genetic analysis of papillary thyroid cancer (PTC) has identified mutations in a large percentage of patients, the genetic basis of follicular thyroid cancer (FTC) is less certain. Thyroid cancer, including both PTC and FTC, has been observed in patients with the inherited tumor predisposition Carney complex, caused by mutations in PRKAR1A. In order to investigate the role of loss of PRKAR1A in thyroid cancer, we generated a tissue-specific knockout of Prkar1a in the thyroid. We report that the resulting mice are hyperthyroid and developed follicular thyroid neoplasms by 1 year of age, including FTC in over 40% of animals. These thyroid tumors showed a signature of pathway activation different from that observed in other models of thyroid cancer. In vitro cultures of the tumor cells indicated that Prkar1a-null thyrocytes exhibited growth factor independence and suggested possible new therapeutic targets. Overall, this work represents the first report of a genetic mutation known to cause human FTC that exhibits a similar phenotype when modeled in the mouse. In addition to our knowledge of the mechanisms of human follicular thyroid tumorigenesis, this model is highly reproducible and may provide a viable mechanism for the further clinical development of therapies aimed at FTC.
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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.