ArticleThe Journal of clinical investigation2001
Primary hyperparathyroidism caused by parathyroid-targeted overexpression of cyclin D1 in transgenic mice.
Article in The Journal of clinical investigation, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 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
67 citing papers in PubMed, 236 citations in OpenAlex.
- Evocalcet improved the PTH-calcium setpoint and suppressed parathyroid proliferation in mice model of primary hyperparathyroidism.Journal of bone and mineral metabolism · 2026Article
- Parathyroid histology in normocalcemic and hypercalcemic primary hyperparathyroidism with hypercalciuric renal stones.Journal of the Endocrine Society · 2026Article
- Parathyroid carcinoma: epidemiology and genetics.Endocrine oncology (Bristol, England) · 2026Review
- Parathyroid glands exhibit reduced parenchymatic chief cells and increased extracellular collagen as a response to a long-term low-phosphorus diet in pigs.Animal nutrition (Zhongguo xu mu shou yi xue hui) · 2025Article
- Molecular mechanism for transcriptional regulation of the parathyroid hormone gene by Epiprofin.The FEBS journal · 2025Article
- [Genetic profiling of parathyroid tumours: lifting the veil of mystery].Problemy endokrinologii · 2025Review
- Phenotype of Parathyroid-targetedJournal of the Endocrine Society · 2024Article
- A Knock-In Mouse Model of theJournal of the Endocrine Society · 2023Article
- Influence of Vitamin D Deficiency on Cyclin D1-Induced Parathyroid Tumorigenesis.Endocrinology · 2023Article
- Molecular and Clinical Spectrum of Primary Hyperparathyroidism.Endocrine reviews · 2023Article
- Establishment and characterization of long-term human primary parathyroid tumor subclones derived from Indian PHPT.3 Biotech · 2023Article
- Immunohistochemical Profile of Parathyroid Tumours: A Comprehensive Review.International journal of molecular sciences · 2022Review
- Parathyroid Hormone Regulates Circulating Levels of Sclerostin and FGF23 in a Primary Hyperparathyroidism Model.Journal of the Endocrine Society · 2022Article
- Molecular Mechanisms of Parathyroid Disorders in Chronic Kidney Disease.Metabolites · 2022Review
- Genetics and Epigenetics of Parathyroid Carcinoma.Frontiers in endocrinology · 2022Review
- Parathyroid Tumors: Molecular Signatures.International journal of molecular sciences · 2021Review
- Etelcalcetide decreases the PTH-calcium setpoint without changing maximum and minimum PTH secretion in mice with primary hyperparathyroidism.Journal of bone and mineral metabolism · 2021Article
- Hormonal regulation of biomineralization.Nature reviews. Endocrinology · 2021Review
- 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
7 more citing papers are in PubMed but not listed here.
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Authors and funding
17 authors at 4 institutions in 2 countries.
Funding
Abstract
The relationship between abnormal cell proliferation and aberrant control of hormonal secretion is a fundamental and poorly understood issue in endocrine cell neoplasia. Transgenic mice with parathyroid-targeted overexpression of the cyclin D1 oncogene, modeling a gene rearrangement found in human tumors, were created to determine whether a primary defect in this cell-cycle regulator can cause an abnormal relationship between serum calcium and parathyroid hormone response, as is typical of human primary hyperparathyroidism. We also sought to develop an animal model of hyperparathyroidism and to examine directly cyclin D1's role in parathyroid tumorigenesis. Parathyroid hormone gene regulatory region--cyclin D1 (PTH--cyclin D1) mice not only developed abnormal parathyroid cell proliferation, but also developed chronic biochemical hyperparathyroidism with characteristic abnormalities in bone and, notably, a shift in the relationship between serum calcium and PTH. Thus, this animal model of human primary hyperparathyroidism provides direct experimental evidence that overexpression of the cyclin D1 oncogene can drive excessive parathyroid cell proliferation and that this proliferative defect need not occur solely as a downstream consequence of a defect in parathyroid hormone secretory control by serum calcium, as had been hypothesized. Instead, primary deregulation of cell-growth pathways can cause both the hypercellularity and abnormal control of hormonal secretion that are almost inevitably linked together in this common disorder.
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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.