ReviewCancer science2009
MEN1 gene and its mutations: basic and clinical implications.
Review in Cancer science, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 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
24 citing papers in PubMed, 42 citations in OpenAlex.
- Article
- Novel germline likely pathogenic frameshift variant of the MEN1 gene contributes to multiple endocrine neoplasia type 1: a case report with review of literature.Endocrine journal · 2025Review
- Familial MEN1 Syndrome with Atypical Renal Features and a Coexisting CLDN16 Variant: A Case Series.Journal of clinical medicine · 2025Article
- Genomic Regions Associated with Respiratory Disease in Holstein Calves in the Southern United States.Genes · 2025Article
- Progress report on multiple endocrine neoplasia type 1.Familial cancer · 2025Review
- Deep Learning Techniques to Characterize theBiomedicines · 2024Article
- The role of menin in bone pathology.Endocrine connections · 2022Review
- Investigating the Effects of Amino Acid Variations in Human Menin.Molecules (Basel, Switzerland) · 2022Article
- Multiple endocrine neoplasia type 1 combined with thyroid neoplasm: A case report and review of literatures.World journal of clinical cases · 2022Article
- Common Variable Immunodeficiency-Associated Cancers: The Role of Clinical Phenotypes, Immunological and Genetic Factors.Frontiers in immunology · 2022Article
- Article
- From Initial Description by Wermer to Present-Day MEN1: What have We Learned?World journal of surgery · 2018Review
- Multiple Endocrine Neoplasia: A Genetically Diverse Group of Familial Tumor Syndromes.Journal of pediatric genetics · 2016Review
- Loss of menin mediated by endothelial cells treated with CoPP is associated with increased maturation of adipocytes.Adipocyte · 2013Article
- A new double substitution mutation in the MEN1 gene: a limited penetrance and a specific phenotype.European journal of human genetics : EJHG · 2013Article
- Menin and GIP are inversely regulated by food intake and diet via PI3/AKT signaling in the proximal duodenum.Nutrition & diabetes · 2012Article
- Expression and subcellular localization of menin in human cancer cells.Experimental and therapeutic medicine · 2012Article
- Correlation of mutant menin stability with clinical expression of multiple endocrine neoplasia type 1 and its incomplete forms.Cancer science · 2011Article
- A new mutation in the menin gene causes the multiple endocrine neoplasia type 1 syndrome with adrenocortical carcinoma.Endocrine · 2011Article
- Molecular alterations in sporadic primary hyperparathyroidism.Genetics research international · 2011Article
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.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Heterozygous germline mutations of the tumor-suppressor gene MEN1 are responsible for multiple endocrine neoplasia type 1 (MEN1), a dominantly inherited familial cancer syndrome characterized by pituitary, parathyroid, and enteropancreatic tumors. Various mutations have been identified throughout the entire gene region in patients with MEN1 and related disorders. Neither mutation hot spot nor phenotype–genotype correlation has been established in MEN1 although some missense mutations may be specifically associated with a phenotype of familial isolated hyperparathyroidism. The gene product menin has been implicated in multiple roles, including gene transcription, maintenance of genomic integrity, and control of cell division and differentiation. These multiple functions are likely to be conferred by association with multiple protein factors. Occurrence of MEN1-causing missense mutations throughout menin also suggests the requirement of multiple binding factors for its full tumor-suppressive activity. The effect of menin depletion is highly tissue specific, but its underlying mechanism remains to be elucidated. A DNA test for MEN1 germline mutations is a useful tool for diagnosis of MEN1 although it needs further improvements
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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.