ReviewClinics (Sao Paulo, Brazil)2012
MENX and MEN4.
Review in Clinics (Sao Paulo, Brazil), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 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.
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Who cites it
20 citing papers in PubMed, 50 citations in OpenAlex.
- Incidence and characterization of spontaneous pituitary neuroendocrine tumors in aged spontaneously hypertensive rats.Scientific reports · 2025Article
- Novel germline variants of CDKN1B and CDKN2C identified during screening for familial primary hyperparathyroidism.Journal of endocrinological investigation · 2023Article
- Multiple endocrine neoplasia type 4: a new member of the MEN family.Endocrine connections · 2023Article
- Model systems in SDHx-related pheochromocytoma/paraganglioma.Cancer metastasis reviews · 2021Review
- p27Cells · 2021Review
- A cancer-associated CDKN1B mutation induces p27 phosphorylation on a novel residue: a new mechanism for tumor suppressor loss-of-function.Molecular oncology · 2021Article
- Familial Hyperparathyroidism.Frontiers in endocrinology · 2021Review
- Bone tissue and mineral metabolism in hereditary endocrine tumors: clinical manifestations and genetic bases.Orphanet journal of rare diseases · 2020Review
- Multiple Endocrine Neoplasia Type 1 (MEN1): An Update and the Significance of Early Genetic and Clinical Diagnosis.Frontiers in endocrinology · 2019Review
- Multiple endocrine neoplasia-like syndrome in 24 baboons (Papio spp.).Journal of medical primatology · 2018Article
- The future: genetics advances in MEN1 therapeutic approaches and management strategies.Endocrine-related cancer · 2017Review
- Multiple Endocrine Neoplasia and Hyperparathyroid-Jaw Tumor Syndromes: Clinical Features, Genetics, and Surveillance Recommendations in Childhood.Clinical cancer research : an official journal of the American Association for Cancer Research · 2017Review
- Loss of p27 expression is associated with MEN1 gene mutations in sporadic parathyroid adenomas.Endocrine · 2017Article
- MEN1, MEN4, and Carney Complex: Pathology and Molecular Genetics.Neuroendocrinology · 2016Review
- Hereditary hyperparathyroidism--a consensus report of the European Society of Endocrine Surgeons (ESES).Langenbeck's archives of surgery · 2015Review
- Somatic alterations of CDKN1B are associated with small bowel neuroendocrine tumors.Cancer genetics · 2015Article
- Article
- Update on pancreatic neuroendocrine tumors.Gland surgery · 2014Review
- A differential diagnosis of inherited endocrine tumors and their tumor counterparts.Clinics (Sao Paulo, Brazil) · 2013Review
- Molecular genetics in primary hyperparathyroidism: the role of genetic tests in differential diagnosis, disease prevention strategy, and therapeutic planning. A 2017 update.Clinical cases in mineral and bone metabolism : the official journal of the Italian Society of Osteoporosis, Mineral Metabolism, and Skeletal DiseasesReview
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Multiple endocrine neoplasias are autosomal dominant disorders characterized by the occurrence of tumors in at least two endocrine glands. Two MEN syndromes have long been known and are well characterized: the MEN type 1 (MEN1) and type 2 (MEN2). These syndromes are caused by germline mutations in the MEN1 and RET genes, respectively, and have a different tumor spectrum. Recently, a variant of the MEN syndromes arose spontaneously in a rat colony and was named MENX. Affected animals consistently develop multiple endocrine tumors, with a spectrum that shares features with both MEN1 and MEN2 human syndromes. Genetic studies identified a germline mutation in the Cdkn1b gene, encoding the p27 cell cycle inhibitor, as the causative mutation for MENX. Capitalizing on these findings, heterozygous germline mutations in the human homologue, CDKN1B, were searched for and identified in patients with multiple endocrine tumors. As a consequence of this discovery, a novel human MEN syndrome, named MEN4, was recognized, which is caused by mutations in p27. Altogether, these studies identified Cdkn1b/CDKN1B as a novel tumor susceptibility gene for multiple endocrine tumors in both rats and humans. Here we review the characteristics of the MENX and MEN4 syndromes and we briefly address the main function of p27 and how they are affected by MENX/4-associated mutations.
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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.