ArticleEndocrine2013
Allelic imbalance in sporadic parathyroid carcinoma and evidence for its de novo origins.
Article in Endocrine, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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.
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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
16 citing papers in PubMed, 36 citations in OpenAlex.
- Genome near-haploidization in CDC73-wildtype parathyroid tumors.Scientific reports · 2026Article
- Molecular and Clinical Spectrum of Primary Hyperparathyroidism.Endocrine reviews · 2023Article
- Genomic Profiling Reveals the Variant Landscape of Sporadic Parathyroid Adenomas in Chinese Population.The Journal of clinical endocrinology and metabolism · 2023Article
- Genomic and transcriptomic profiling reveal molecular characteristics of parathyroid carcinoma.Experimental & molecular medicine · 2023Article
- Secondary Mediastinal Bleeding Caused by Parathyroid Adenocarcinoma: A Case Report.Clinical medicine insights. Case reports · 2023Article
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- Hsa_circ_0005729 enhances accuracy in diagnosing parathyroid carcinoma.Endocrine connections · 2022Article
- Molecular analysis of cyclin D1 modulators PRKN and FBX4 as candidate tumor suppressors in sporadic parathyroid adenomas.Endocrine connections · 2021Article
- Genetic Alteration Profiles and Clinicopathological Associations in Atypical Parathyroid Adenoma.International journal of genomics · 2021Article
- Clinical and Molecular Genetics of Primary Hyperparathyroidism.Hormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et metabolisme · 2020Review
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- Article
- Coronary Heart Disease and an Incidental Parathyroid Carcinoma.Case reports in pathology · 2019Article
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- Update on parathyroid carcinoma.Journal of endocrinological investigation · 2016Review
- Genetic and epigenetic changes in sporadic endocrine tumors: parathyroid tumors.Molecular and cellular endocrinology · 2014Review
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
Abstract
Parathyroid cancer is a rare, clinically aggressive cause of primary hyperparathyroidism, and whether these malignancies generally evolve from pre-existing benign adenomas or arise de novo is unclear. Furthermore, while inactivation of the CDC73 (HRPT2) tumor suppressor gene, encoding parafibromin, is a major contributor, other genes essential to parathyroid carcinogenesis remain unknown. We sought to identify genomic regions potentially harboring such oncogenes or tumor suppressor genes, and to gain insight into the origins and molecular relationship of malignant versus benign parathyroid tumors. We performed genome-wide copy-number and loss of heterozygosity analysis using Affymetrix 50K SNP mapping arrays and/or comparative genomic hybridization on 16 primary parathyroid carcinomas, local recurrences or distant metastases, and matched normal controls, from 10 individuals. Recurrent regions of allelic loss were observed on chromosomes 1p, 3, and 13q suggesting that key parathyroid tumor suppressor genes are located in these chromosomal locations. Recurrent allelic gains were seen on chromosomes 1q and 16, suggesting the presence of parathyroid oncogenes on these chromosomes. Importantly, the most common alteration in benign parathyroid adenomas, loss of 11q, was not found as a recurrent change in the malignant parathyroid tissues. Molecular allelotyping using highly polymorphic microsatellite markers provided further confirmation that the prevalence of 11q loss is markedly and significantly lower in carcinomas as compared with adenomas. Our observations provide molecular support for the concept that sporadic parathyroid cancer usually arises de novo, rather than evolving from a pre-existing typical benign adenoma. Furthermore, these results help direct future investigation to ultimately determine which of the candidate genes in these chromosomal locations make significant contributions to the molecular pathogenesis of parathyroid cancer.
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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.