Selected markers of proliferation and apoptosis in the parathyroid lesions: a spatial visualization and quantification.

Journal of Molecular Histology
Elzbieta KaczmarekAndrzej Kluk

Abstract

The aim of the paper was to apply a method for quantitative assessment of proliferation and apoptosis markers, based on their 3D visualization, in cases of parathyroid adenoma and hyperplasia. Material was obtained from 49 patients (32 females and 17 males) with primary hyperparahyroidism. Quantitative immunohistochemistry studies of Ki-67, proliferating cell nuclear antigen (PCNA) and bcl-2 were performed on digital microscopy images with the use of 3D visualization. The use of spatial visualization method allowed us to perform objective quantitative assessment of the studied immunohistochemical markers. The average cell nuclear fraction of Ki67+ was 1.8% in hyperplasia and 1.9% in adenoma cases while 3.5% in the controls. The highest expression of PCNA was found in parathyroid hyperplasia (22.9%) and significantly decreased in adenoma (12.5%) and in the control group (16.8%). The lower expression of bcl-2 in hyperplasia cases (mean area fraction of 0.172 per 1 mum(2), in contrast to 0.643 in adenomas and 0.648 in control) suggested that principal cells can be ready for apoptosis and may confirm the important role of bcl-2 protein in etiopathogenesis of hyperplasia of the parathyroid gland while PCNA might be a useful marker f...Continue Reading

References

Sep 1, 1986·Controlled Clinical Trials·R DerSimonian, N Laird
Nov 1, 1996·APMIS : Acta Pathologica, Microbiologica, Et Immunologica Scandinavica·W WangL Grimelius
May 20, 1998·Journal of Endocrinological Investigation·A G NaccaratoP Viacava
Dec 19, 1998·The Journal of Histochemistry and Cytochemistry : Official Journal of the Histochemistry Society·H A LehrA M Gown
Sep 29, 1999·Statistical Methods in Medical Research·J M Bland, D G Altman
Jun 6, 2000·Experimental Cell Research·E Endl, J Gerdes
May 29, 2003·American Journal of Respiratory and Critical Care Medicine·Jacob K SontUNKNOWN Asthma Management Project University of Leiden Study Group
Jun 28, 2003·Journal of Cell Science·Giovanni Maga, Ulrich Hubscher
Dec 17, 2003·Journal of Gastroenterology and Hepatology·Gamal M DahabOsama A Sharaf El-Din
May 11, 2004·Urologia Internationalis·Maria Luisa Brandi, Alberto Falchetti
Apr 1, 2005·Pathology Oncology Research : POR·Tuvia HadarRumelia Koren
Dec 7, 2007·Clinical Cancer Research : an Official Journal of the American Association for Cancer Research·Jean-Simon DialloFred Saad

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Citations

Dec 24, 2013·Pathology, Research and Practice·Elzbieta KaczmarekMichał Drews
Nov 1, 2011·Nephrology, Dialysis, Transplantation : Official Publication of the European Dialysis and Transplant Association - European Renal Association·Gerald MillerCharles M Henley
Feb 23, 2011·The Journal of Histochemistry and Cytochemistry : Official Journal of the Histochemistry Society·Shan-Rong ShiClive R Taylor
Nov 8, 2011·Domestic Animal Endocrinology·R-J BaiW Tian
Apr 1, 2017·Journal of Investigative Surgery : the Official Journal of the Academy of Surgical Research·Oliwia Anna SegietRomuald Wojnicz
Jun 19, 2010·American Journal of Respiratory Cell and Molecular Biology·Tanveer AhmadAnurag Agrawal

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