ReviewNeuroendocrinology2016
MEN1, MEN4, and Carney Complex: Pathology and Molecular Genetics.
Review in Neuroendocrinology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
27 citing papers in PubMed, 95 citations in OpenAlex.
- Revisiting parathyroid carcinoma through the lens of the 2022 WHO classification.Hormones (Athens, Greece) · 2026Article
- Large Right Atrial Myxoma With Endocrine Abnormalities as a Possible Case of a Syndromic Disease: A Case Report.Clinical case reports · 2025Article
- Childhood Multiple Endocrine Neoplasia (MEN) Syndromes: Genetics, Clinical Heterogeneity and Modifying Genes.Journal of clinical medicine · 2024Review
- Syndromic MEN1 parathyroid adenomas consist of both subclonal nodules and clonally independent tumors.Virchows Archiv : an international journal of pathology · 2024Article
- Article
- Novel germline variants of CDKN1B and CDKN2C identified during screening for familial primary hyperparathyroidism.Journal of endocrinological investigation · 2023Article
- Association Between Parafibromin Expression and Presence of Brown Tumors and Jaw Tumors in Patients with Primary Hyperparathyroidism: Series of Cases with Review of the Literature.The American journal of case reports · 2022Review
- Review
- Overview of the 2022 WHO Classification of Parathyroid Tumors.Endocrine pathology · 2022Review
- Overview of the 2022 WHO Classification of Familial Endocrine Tumor Syndromes.Endocrine pathology · 2022Review
- Quantitative proteomics revealed the molecular characteristics of distinct types of granulated somatotroph adenomas.Endocrine · 2021Article
- [Neuroendorine paraneoplastic syndromes].Der Hautarzt; Zeitschrift fur Dermatologie, Venerologie, und verwandte Gebiete · 2021Review
- Recent Understanding and Future Directions of Recurrent Corticotroph Tumors.Frontiers in endocrinology · 2021Review
- Hereditary Parathyroid Disease: Sometimes Pathologists Do Not Know What They Are Missing.Endocrine pathology · 2020Review
- Pathology of prolactinomas: any predictive value?Pituitary · 2020Review
- Hyperprolactinaemia.Journal of clinical medicine · 2019Review
- The Clinicopathological Spectrum of Acromegaly.Journal of clinical medicine · 2019Review
- An update on the genetics of benign pituitary adenomas in children and adolescents.Current opinion in endocrine and metabolic research · 2018Article
- Growth hormone-producing pituitary adenomas in childhood and young adulthood: clinical features and outcomes.Pituitary · 2018Article
- Recent advances in understanding corticotroph pituitary tumor initiation and progression.F1000Research · 2018Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
Abstract
Pituitary adenomas are a common feature of a subset of endocrine neoplasia syndromes, which have otherwise highly variable disease manifestations. We provide here a review of the clinical features and human molecular genetics of multiple endocrine neoplasia (MEN) type 1 and 4 (MEN1 and MEN4, respectively) and Carney complex (CNC). MEN1, MEN4, and CNC are hereditary autosomal dominant syndromes that can present with pituitary adenomas. MEN1 is caused by inactivating mutations in the MEN1 gene, whose product menin is involved in multiple intracellular pathways contributing to transcriptional control and cell proliferation. MEN1 clinical features include primary hyperparathyroidism, pancreatic neuroendocrine tumours and prolactinomas as well as other pituitary adenomas. A subset of patients with pituitary adenomas and other MEN1 features have mutations in the CDKN1B gene; their disease has been called MEN4. Inactivating mutations in the type 1α regulatory subunit of protein kinase A (PKA; the PRKAR1A gene), that lead to dysregulation and activation of the PKA pathway, are the main genetic cause of CNC, which is clinically characterised by primary pigmented nodular adrenocortical disease, spotty skin pigmentation (lentigines), cardiac and other myxomas and acromegaly due to somatotropinomas or somatotrope hyperplasia.
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What 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.