Document Detail


Immunohistochemical detection of cell cycle regulators, Fhit protein and apoptotic cells in parathyroid lesions.
MedLine Citation:
PMID:  12534361     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
OBJECTIVE: The pathological distinction between parathyroid neoplasms and hyperplasias remains difficult. Changes in cell cycle control may lead to clonal proliferation and precede tumorigenesis. The parathyroid adenoma 1 oncogene, subsequently identified as the gene encoding cyclin D1, has been shown to be important to parathyroid tumour development. In addition to cell proliferation, the mechanisms of parathyroid cell turnover include apoptosis. The tumour-suppressor activity of the fragile histidine triad gene (FHIT) is linked to its proapoptotic function and cell cycle control. We attempted to evaluate the cellular proliferative kinetics and apoptotic function of the parathyroid glands in patients with non-familial hyperparathyroidism (HPT). DESIGN: TIssue specimens were taken from 40 patients with primary HPT (17 adenomas, two carcinomas and 21 primary hyperplasias) and from 30 patients with secondary HPT. Normal glands served as controls. METHODS: In a standard immunohistochemical procedure, monoclonal antibodies to Ki-67 antigen and single-stranded DNA were applied to detect cycling and apoptotic cells respectively; polyclonal antibodies to cyclin D1 and Fhit protein were used. Immunostaining was estimated by image analysis and statistical analysis was subsequently performed. RESULTS: Significantly higher proliferative and apoptotic indexes were detected in the diseased glands in comparison with normal controls. In neoplastic and secondarily hyperplastic glands, apoptotic indexes were higher than in primarily hyperplastic glands; the difference between neoplastic and primarily hyperplastic glands was statistically significant (P=0.034). Cyclin D1 was overexpressed in a considerable proportion of tumours (68.4%). A reduction of Fhit protein immunoreactivity was selectively noticed in carcinomas. CONCLUSIONS: In primary hyperplasia, the remarkable proliferation of parathyroid glands may be due to the reduction of the apoptotic process. FHIT gene abnormalities are worthy of investigation in parathyroid carcinogenesis.
Authors:
G-E Thomopoulou; S Tseleni-Balafouta; A C Lazaris; H Koutselini; N Kavantzas; P S Davaris
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  European journal of endocrinology / European Federation of Endocrine Societies     Volume:  148     ISSN:  0804-4643     ISO Abbreviation:  Eur. J. Endocrinol.     Publication Date:  2003 Jan 
Date Detail:
Created Date:  2003-01-21     Completed Date:  2003-02-24     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  9423848     Medline TA:  Eur J Endocrinol     Country:  England    
Other Details:
Languages:  eng     Pagination:  81-7     Citation Subset:  IM    
Affiliation:
Department of Pathology, School of Medicine, The Athens National and Kapodistrian University, Athens, Greece.
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MeSH Terms
Descriptor/Qualifier:
Acid Anhydride Hydrolases*
Adenoma / chemistry,  pathology
Apoptosis*
Carcinoma / chemistry,  pathology
Cell Cycle
Female
Humans
Hyperparathyroidism / pathology*
Hyperplasia
Immunohistochemistry
Ki-67 Antigen / analysis
Male
Middle Aged
Neoplasm Proteins / analysis*
Parathyroid Glands / chemistry*,  pathology*
Parathyroid Neoplasms / chemistry,  pathology
Chemical
Reg. No./Substance:
0/Ki-67 Antigen; 0/Neoplasm Proteins; 0/fragile histidine triad protein; EC 3.6.-/Acid Anhydride Hydrolases

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