ArticleTransactions of the American Clinical and Climatological Association2016
MAJOR MOLECULAR GENETIC DRIVERS IN SPORADIC PRIMARY HYPERPARATHYROIDISM.
Article in Transactions of the American Clinical and Climatological Association, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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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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Who cites it
5 citing papers in PubMed, 10 citations in OpenAlex.
- Sporadic parathyroid adenoma: an updated review of molecular genetics.Frontiers in endocrinology · 2023Review
- Integrated Whole-Exome and Transcriptome Sequencing of Sporadic Parathyroid Adenoma.Frontiers in endocrinology · 2021Article
- In vitroMicroorganisms · 2020Article
- Whole exome sequencing in familial isolated primary hyperparathyroidism.Journal of endocrinological investigation · 2020Article
- Proteomics Analysis of Tissue Samples Reveals Changes in Mitochondrial Protein Levels in Parathyroid Hyperplasia over Adenoma.Cancer genomics & proteomicsArticle
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
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Abstract
Primary hyperparathyroidism is primarily due to a solitary parathyroid adenoma but multi-gland disease, parathyroid carcinoma, and ectopic parathyroid hormone production can occur. Although primary hyperparathyroidism mostly presents sporadically, strong familial predispositions also exist. Much is known about heritable genetic mutations responsible for these syndromes, including multiple endocrine neoplasia types 1 and 2A, hyperparathyroidism-jaw tumor syndrome, and familial hypocalciuric hypercalcemia. Acquired mutations in common sporadic hyperparathyroidism have also been discovered. Here we focus on the most common and well-established genetic drivers: 1) involvement of the oncogene cyclin D1 in human neoplasia was first established in parathyroid adenomas, followed by recognition of its importance in other tumor types including breast cancer and B-lymphoid malignancy; and 2) somatic mutation of the
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Identifiers
28066056PMC5216514W2579578764What OpenQuestion holds
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.