ECE2014 Poster Presentations Endocrine tumours and neoplasia (99 abstracts)
1Department of Histology and Embryology, Medical University of Silesia in Katowice, 41-808 Zabrze, ul. Jordana 19, Poland; 2Chair and Clinical Department of General Surgery, Medical University of Silesia in Katowice, 41-902 Bytom, ul. Batorego 15, Poland.
Background: Proliferating cell nuclear antigen (PCNA) is a cell cycle marker protein. It interacts with more than 100 proteins involved in DNA replication, DNA repair, cell cycle control, chromatin remodeling/epigenetic inheritance, chromatid cohesion and transcription. Cyclin-dependent kinase 1 (Cdk1) is a serine/threonine protein kinase which regulates diverse cell cycle transitions (G1/S, S and G2/M phases) and associates with different cell-cycle stage-specific cyclins. Both of these proteins could be potentially useful in diagnosis of primary hyperparathyroidism which is one of the most common endocrine disorders caused by adenoma (80%), hyperplasia (15%) and carcinoma (5%).
Aim: The aim of the study was to assess the immunohistochemical expression of PCNA and Cdk1 as a potentially useful in diagnosis of hyperplastic lesions of the parathyroid glands.
Methods: For immunohistochemistry, parathyroid specimens of patients undertaken surgery due to primary hyperparathyroidism caused by adenoma and primary hyperplasia were investigated. Frozen sections were incubated with purified mouse monoclonal antihuman antibodies: anti-PCNA (clone 24/PCNA) and anti-Cdk1 (clone 1/Cdk1/Cdc2) from BD Biosciences. The immunohistological investigations were performed by the BrightVision method from ImmunoLogic. The number of proliferating cells were counted and expressed as a mean value of at least six counted high power fields (HPF, ×400). The sections were counterstained with Mayers haematoxylin.
Results: Positive Cdk1 immunoreaction was significantly increased in parathyroid adenomas, whereas PCNA was considerably lower in adenomas and hyperplasias compared to healthy parathyroid glands. Positively stained cells were localized in the well vascularized region of the parathyroid nodule.
Conclusion: Numerous different mechanisms are responsible for hyperplastic changes: activation of oncogenes, inactivation of tumor-suppressor genes, epigenetic changes and disturbance of the balance between growth factors and other transmitter substances including proteins involved in cell cycle regulation.