ArticleEndocrine2004
Clinical and genetic features of patients with multiple endocrine tumors who have neither family history nor MEN1 germline mutations.
Article in Endocrine, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed, 9 citations in OpenAlex.
- A Japanese Family Meeting the Clinical Diagnostic Criteria for MEN1 with a MEN1 Variant of Uncertain Significance.Internal medicine (Tokyo, Japan) · 2024Article
- Germ-line mutations in p27Kip1 cause a multiple endocrine neoplasia syndrome in rats and humans.Proceedings of the National Academy of Sciences of the United States of America · 2006Article
- Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Multiple endocrine neoplasia type 1 (MEN1) is an hereditary tumor syndrome that involves specific endocrine organs such as parathyroids, anterior pituitary gland, and endocrine pancreas. The responsible gene for this syndrome, MEN1, has been isolated and that enabled genetic diagnosis for patients with endocrine tumors and early detection of asymptomatic gene carriers in affected families. Nevertheless, there are a considerable number of patients with MEN1 who have neither family history nor germline MEN1 mutations. In this article, clinical features of such patients are described. Among 53 MEN1 patients we have seen during the last 20 yr, five patients who did not have either MEN1 germline mutation or family history were categorized as MEN1 phenocopy. During the same period, we have also experienced three patients who had primary hyperparathyroidism and adrenocortical tumor but had no apparent family history of endocrine tumors. These patients were considered as MEN1 phenocopy variants and included in the study. The mean age of MEN1 phenocopy patients (including variants) at diagnosis was 48 yr, which was not significantly different from that of probands of familial MEN1 (46 yr) who carry heterozygous MEN1 gene mutations. In the majority of MEN1 phenocopy patients, primary hyperparathyroidism was due to a single parathyroid adenoma. In contrast to a previous report, we found that MEN1 phenocopy patients are not necessarily older than probands of familial MEN1. Phenotypic expression of such patients is variable, thus differentiation of familial MEN1 and MEN1 phenocopy cannot be made based on age and clinical phenotype alone.
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