ReviewFrontiers of hormone research2013
Multiple endocrine neoplasia type 1.
Review in Frontiers of hormone research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 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
28 citing papers in PubMed, 73 citations in OpenAlex.
- Adrenal Incidentaloma: From Silent Diagnosis to Clinical Challenge.Biomedicines · 2025Review
- Molecular Pathophysiology of Parathyroid Tumorigenesis-The Lesson from a Rare Disease: The "MEN1 Model".International journal of molecular sciences · 2024Review
- Prospective Genetic Screening in Multiple Endocrine Neoplasia Syndromes.Children (Basel, Switzerland) · 2024Review
- Tall stature and gigantism in transition age: clinical and genetic aspects-a literature review and recommendations.Journal of endocrinological investigation · 2024Review
- Clinically Defined Mutations inCancer research communications · 2023Article
- Primary bilateral macronodular adrenal hyperplasia: definitely a genetic disease.Nature reviews. Endocrinology · 2022Review
- Thymoma (World Health Organization Type AB) in multiple endocrine neoplasia type 1: a case report.Journal of surgical case reports · 2022Article
- Multiple endocrine neoplasia type 1: a new germline "homozygous" variant (c.201delC) caused by detection errors.Hereditary cancer in clinical practice · 2022Article
- Somatostatin Analogue Therapy in MEN1-Related Pancreatic Neuroendocrine Tumors from Evidence to Clinical Practice: A Systematic Review.Pharmaceuticals (Basel, Switzerland) · 2021Review
- Bilateral Adrenal Hyperplasia: Pathogenesis and Treatment.Biomedicines · 2021Review
- Multiple Endocrine Neoplasia Type 1: The Potential Role of microRNAs in the Management of the Syndrome.International journal of molecular sciences · 2020Review
- Article
- A large Turkish pedigree with multiple endocrine neoplasia type 1 syndrome carrying a rare mutation: c.1680_1683 del TGAG.The Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology · 2020Article
- Phenotypes Associated With MEN1 Syndrome: A Focus on Genotype-Phenotype Correlations.Frontiers in endocrinology · 2020Review
- Could the Less-Than Subtotal Parathyroidectomy Be an Option for Treating Young Patients With Multiple Endocrine Neoplasia Type 1-Related Hyperparathyroidism?Frontiers in endocrinology · 2019Article
- Long Noncoding RNA MEG3 Is an Epigenetic Determinant of Oncogenic Signaling in Functional Pancreatic Neuroendocrine Tumor Cells.Molecular and cellular biology · 2017Article
- The future: genetics advances in MEN1 therapeutic approaches and management strategies.Endocrine-related cancer · 2017Review
- Genetics of multiple endocrine neoplasia type 1 syndrome: what's new and what's old.F1000Research · 2017Review
- Long-Term Surveillance of Treated Hyperparathyroidism for Multiple Endocrine Neoplasia Type 1: Recurrence or Hypoparathyroidism?World journal of surgery · 2016Article
- Mouse models of adrenocortical tumors.Molecular and cellular endocrinology · 2016Review
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
Multiple endocrine neoplasia type 1 (MEN1) is an autosomal-dominant tumor syndrome characterized by the occurrence of tumors in multiple endocrine tissues and nonendocrine tissues. The three main endocrine tissues most frequently affected by tumors are parathyroid (95%), enteropancreatic neuroendocrine (50%) and anterior pituitary (40%). Tumors are caused by a heterozygous germline-inactivating mutation in the MEN1 gene (1st hit) followed by somatic inactivating mutation or loss of the normal copy of the gene (2nd hit), leading to complete loss of function of the encoded protein menin. Most of the disease features and tumors are recapitulated in mouse models with heterozygous germline loss of the Men1 gene. Also, tissue-specific tumors are observed in mouse models with homozygous somatic loss of the Men1 gene specifically in MEN1-associated endocrine tissues. Hence, mouse models could serve as possible surrogates for studying MEN1 and related states. To gain insights into MEN1 pathophysiology, menin-interacting partners and pathways have been identified to investigate its tumor suppressor and other functions. Also, the 3D crystal structure of menin has been deciphered which could be useful to reveal the relevance of MEN1 gene mutations and menin's interactions. This chapter covers clinical, genetic and basic findings about the MEN1 syndrome, MEN1 gene and its product protein menin.
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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.