ArticleGenetics research international2011
Molecular alterations in sporadic primary hyperparathyroidism.
Article in Genetics research international, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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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Who cites it
7 citing papers in PubMed, 17 citations in OpenAlex.
- Parathyroid carcinoma: epidemiology and genetics.Endocrine oncology (Bristol, England) · 2026Review
- Engineered nanoparticles for endocrine tumor targeting, current progress and future outlook.Medical oncology (Northwood, London, England) · 2025Review
- PARATHYROID CARCINOMA: ULTRASONOGRAPHIC AND CLINICAL EXPERIENCE.Acta clinica Croatica · 2023Article
- Genetics and Epigenetics of Parathyroid Carcinoma.Frontiers in endocrinology · 2022Review
- Parathyroid Tumors: Molecular Signatures.International journal of molecular sciences · 2021Review
- Differential expression of miRNA199b-5p as a novel biomarker for sporadic and hereditary parathyroid tumors.Scientific reports · 2018Article
- Translational research in endocrine surgery.Surgical oncology clinics of North America · 2013Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Primary hyperparathyroidism (PHPT) is a frequent endocrine disorder characterized by an excessive autonomous production and release of parathyroid hormone (PTH) by the parathyroid glands. This endocrinopathy may result from the development of a benign lesion (adenoma or hyperplasia) or from a carcinoma. Most of the PHPT cases occur sporadically; however, approximately 10% of the patients present a familial form of the disease. The molecular mechanisms underlying the pathogenesis of sporadic PHPT are incompletely understood, even though somatic alterations in MEN1 gene and CCND1 protein overexpression are frequently observed. The MEN1 gene is mutated in about 30% of the parathyroid tumours and the protooncogene CCND1 is implicated in parathyroid neoplasia by rearrangements, leading to an overexpression of CCND1 protein in parathyroid cells. The aim of this work is to briefly update the molecular alterations underlying sporadic primary hyperparathyroidism.
Identifiers
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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.