ArticleThe American journal of pathology2001
Deletion of 11q23 and cyclin D1 overexpression are frequent aberrations in parathyroid adenomas.
Article in The American journal of pathology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 79 citations in OpenAlex.
- KMT2A and chronic inflammation as potential drivers of sporadic parathyroid adenoma.Clinical and translational medicine · 2024Article
- Molecular and Clinical Spectrum of Primary Hyperparathyroidism.Endocrine reviews · 2023Article
- Analysis of CCND1 protein and circulatory antioxidant enzyme activity association in oral squamous cell carcinoma.Saudi journal of biological sciences · 2021Article
- Molecular analysis of cyclin D1 modulators PRKN and FBX4 as candidate tumor suppressors in sporadic parathyroid adenomas.Endocrine connections · 2021Article
- Intratumor heterogeneity in human parathyroid tumors.Histology and histopathology · 2020Review
- Clinical and Molecular Genetics of Primary Hyperparathyroidism.Hormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et metabolisme · 2020Review
- Clinical Impact of p27Endocrine pathology · 2018Article
- Immunohistochemistry in Diagnostic Parathyroid Pathology.Endocrine pathology · 2018Review
- Computational identification of micro-structural variations and their proteogenomic consequences in cancer.Bioinformatics (Oxford, England) · 2018Article
- Diagnosis, management, histology and genetics of sporadic primary hyperparathyroidism: old knowledge with new tricks.Endocrine connections · 2018Review
- Genetics of Hyperparathyroidism, Including Parathyroid Cancer.Endocrinology and metabolism clinics of North America · 2017Review
- Primary Hyperparathyroidism Focused on Molecular Pathogenesis.European endocrinology · 2014Review
- ATM deficiency augments constitutively nuclear cyclin D1-driven genomic instability and lymphomagenesis.Oncogene · 2014Article
- Genetic characterization of large parathyroid adenomas.Endocrine-related cancer · 2012Article
- Impaired nuclear export of tumor-derived c-terminal truncated cyclin D1 mutant in ESCC cancer.Oncology letters · 2011Article
- Cell cyclins: triggering elements of cancer or not?World journal of surgical oncology · 2010Review
- Clinical and molecular genetics of parathyroid neoplasms.Best practice & research. Clinical endocrinology & metabolism · 2010Review
- Nuclear accumulation of cyclin D1 during S phase inhibits Cul4-dependent Cdt1 proteolysis and triggers p53-dependent DNA rereplication.Genes & development · 2007Article
- DNA copy number changes in young gastric cancer patients with special reference to chromosome 19.British journal of cancer · 2003Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hyperparathyroidism may result from parathyroid hyperplasia or adenoma, or rarely from parathyroid carcinoma. Pericentromeric inversion of chromosome 11 that results in activation of the P:RAD1/cyclin D1 gene and tumor suppressor gene loss have been described as genetic abnormalities in the evolution of parathyroid neoplasms. We studied tissue samples taken from primary parathyroid hyperplasia, parathyroid adenoma, and histologically normal parathyroid tissue by comparative genomic hybridization, fluorescent in situ hybridization, and immunohistochemistry for cyclin D1. DNA copy number changes were infrequent in primary hyperplasia (4 of 24, 17%), but common in adenomas (10 of 16, 63%; P: = 0.0059). The most common change was deletion of the entire chromosome 11 or a part of it, with a minimal common region at 11q23. This change was present in five (31%) adenomas and two (8%) primary hyperplasias. Fluorescent in situ hybridization confirmed the presence of both MEN1 alleles located at 11q13 despite deletion of 11q23 in all three cases studied. Cyclin D1 was overexpressed in six (40%) of the 15 adenomas studied, whereas none of the 27 hyperplasias (P: = 0.0010) nor the five histologically normal tissue samples overexpressed cyclin D1. Either DNA copy number loss or cyclin D1 overexpression was present in 13 (81%) of the 16 adenomas. We conclude that DNA copy number loss and cyclin D1 overexpression are common in parathyroid adenomas. The region 11q23 is frequently lost in parathyroid adenomas and occasionally in parathyroid hyperplasias, and this suggests the possibility that a tumor suppressor gene that is important in their pathogenesis is present on 11q23.
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