ArticlePathology oncology research : POR2012
Molecular profiling of parathyroid hyperplasia, adenoma and carcinoma.
Article in Pathology oncology research : POR, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 38 citations in OpenAlex.
- Molecular and Clinical Spectrum of Primary Hyperparathyroidism.Endocrine reviews · 2023Article
- Sporadic parathyroid adenoma: an updated review of molecular genetics.Frontiers in endocrinology · 2023Review
- Gene expression and methylation profiles show the involvement of POMC in primary hyperparathyroidsm.Journal of translational medicine · 2022Article
- Immunohistochemical Profile of Parathyroid Tumours: A Comprehensive Review.International journal of molecular sciences · 2022Review
- Role of Ca²⁺ in Inhibiting Ischemia-Induced Apoptosis of Parathyroid Gland Cells in New Zealand White Rabbits.Medical science monitor : international medical journal of experimental and clinical research · 2020Article
- Using a Novel Diagnostic Nomogram to Differentiate Malignant from Benign Parathyroid Neoplasms.Endocrine pathology · 2019Article
- Immunohistochemistry in Diagnostic Parathyroid Pathology.Endocrine pathology · 2018Review
- Diagnosis, management, histology and genetics of sporadic primary hyperparathyroidism: old knowledge with new tricks.Endocrine connections · 2018Review
- Predictors of multiglandular disease in primary hyperparathyroidism.Langenbeck's archives of surgery · 2018Article
- Parafibromin, galectin-3, PGP9.5, Ki67, and cyclin D1: using an immunohistochemical panel to aid in the diagnosis of parathyroid cancer.World journal of surgery · 2014Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The objective of the study was to examine proliferation and apoptosis associated gene expression in the whole sequence parathyroid lesions to reveal specific features of carcinoma. This study was based on surgically removed parathyroid tissues, gene expression analysis was performed both at gene and protein level. First, mRNA isolation was performed from deep-frozen tissue samples, and further apoptosis pathway-specific cDNA macroarray analysis was carried out. The results were validated with real-time PCR. Subsequently, protein expression was analyzed with immunhistochemistry on Tissue Micro Array multi-blocks derived from several paraffin-embedded samples. cDNA macroarrays revealed elevated expression of both pro-apoptotic (FAS receptor, TRAIL ligand, CASPASE8, and -4) and anti-apoptotic (cIAP1, APOLLON) genes in benign proliferative lesions compared to that in normal gland. TMA studies showed overexpression of KI67, P53, SURVIVIN and APOLLON protein and failure of expression of P27, BCL2, BAX, CHROMOGRANIN-A, SYNAPTOPHYSIN, CYCLIND1, FLIP, TRAIL, CK8, CK18, CK19 in parathyroid carcinoma was detected. These alterations in gene expression of the investigated products could be used in differentiation between beningn and malignant proliferative processes of the parathyroid gland. Authors conclude that a series of alterations in gene expression such as overexpression of APOLLON, P53, KI67 and suppression of P27, BCL2, BAX lead to uncontrolled cell proliferation, but still not leading to increased apoptotic activity in parathyroid carcinoma.
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Registered trials
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