ArticleCancers2020
Comprehensive Analysis of MEN1 Mutations and Their Role in Cancer.
Article in Cancers, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
21 citing papers in PubMed, 33 citations in OpenAlex.
- The germline landscape of pituitary adenomas: established and emerging predisposition genes.The Journal of clinical endocrinology and metabolism · 2026Review
- CRISPR base editor screening identifies spectrum of MEN1 mutations impacting menin inhibitors in clinical trials.Nature communications · 2026Article
- Two novel multiple endocrine neoplasia type 1 variants caused thymic neuroendocrine tumor: a case report.Hereditary cancer in clinical practice · 2026Article
- Epidemiology and clinical outcomes of clinically suspected multiple endocrine neoplasia type 1 in South Korea: a nationwide cohort study.Frontiers in endocrinology · 2025Article
- Molecular Pathophysiology of Parathyroid Tumorigenesis-The Lesson from a Rare Disease: The "MEN1 Model".International journal of molecular sciences · 2024Review
- Unlocking the Genetic Secrets of Acromegaly: Exploring the Role of Genetics in a Rare Disorder.Current issues in molecular biology · 2024Review
- Turning Points in Cross-Disciplinary Perspective of Primary Hyperparathyroidism and Pancreas Involvements: Hypercalcemia-Induced Pancreatitis,International journal of molecular sciences · 2024Review
- Article
- Alternative splicing generates isoform diversity inEndocrine oncology (Bristol, England) · 2024Article
- Novel MEN1-associated retroperitoneal pleomorphic liposarcoma.Rare tumors · 2024Article
- Blood-based Proteomic Signatures Associated With MEN1-related Duodenopancreatic Neuroendocrine Tumor Progression.The Journal of clinical endocrinology and metabolism · 2023Article
- Dependency of B-Cell Acute Lymphoblastic Leukemia and Multiple Myeloma Cell Lines on MEN1 Extends beyond MEN1-KMT2A Interaction.International journal of molecular sciences · 2023Article
- Investigating the novel-binding site of RPA2 on Menin and predicting the effect of point mutation of Menin through protein-protein interactions.Scientific reports · 2023Article
- A Novel PathogenicJCEM case reports · 2023Article
- Evaluating the role of MEN1 gene expression and its clinical significance in breast cancer patients.PloS one · 2023Article
- Gene Mutations in Cushing's Syndrome.Molecular syndromology · 2023Review
- Identification of New Molecular Biomarkers in Ovarian Cancer Using the Gene Expression Profile.Journal of clinical medicine · 2022Article
- A Hypoxia-Induced SCFFBXL1 E3 Ligase Ubiquitinates and Degrades the MEN1 Tumor Suppressor to Promote Colorectal Cancer Tumorigenesis.Cancer research and treatment · 2022Article
- Investigating the Effects of Amino Acid Variations in Human Menin.Molecules (Basel, Switzerland) · 2022Article
- Comprehensive Genetic Analysis of DGAT2 Mutations and Gene Expression Patterns in Human Cancers.Biology · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
MENIN is a scaffold protein encoded by the MEN1 gene that functions in multiple biological processes, including cell proliferation, migration, gene expression, and DNA damage repair. MEN1 is a tumor suppressor gene, and mutations that disrupts MEN1 function are common to many tumor types. Mutations within MEN1 may also be inherited (germline). Many of these inherited mutations are associated with a number of pathogenic syndromes of the parathyroid and pancreas, and some also predispose patients to hyperplasia. In this study, we cataloged the reported germline mutations from the ClinVar database and compared them with the somatic mutations detected in cancers from the Catalogue of Somatic Mutations in Cancer (COSMIC) database. We then used statistical software to determine the probability of mutations being pathogenic or driver. Our data show that many confirmed germline mutations do not appear in tumor samples. Thus, most mutations that disable MEN1 function in tumors are somatic in nature. Furthermore, of the germline mutations that do appear in tumors, only a fraction has the potential to be pathogenic or driver mutations.
Indexed as
Identifiers
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.