Document Detail

The expression of calcitonin receptor detected in malignant cells of the brain tumour glioblastoma multiforme and functional properties in the cell line A172.
MedLine Citation:
PMID:  22335784     Owner:  NLM     Status:  Publisher    
Wookey P J, McLean C A, Hwang P, Furness S G B, Nguyen S, Kourakis A, Hare D L & Rosenfeld J V (2012) Histopathology The expression of calcitonin receptor detected in malignant cells of the brain tumour glioblastoma multiforme and functional properties in the cell line A172 Aim:  Previous studies have indicated that expression of calcitonin receptor (CTR) could be induced in a proinflammatory environment. In the present study, CTR-immunoreactivity (CTR-ir) was investigated in brain tissue from patients with glioblastoma multiforme (GBM). Methods and results:  In immunohistochemical analysis of GBM samples, tissues with complex glomeruloid structures surrounded by malignant cells were analysed for CTR-ir using anti-human CTR antibodies generated against two separate epitopes of CTR. CTR-ir was associated predominantly with glial cells. Regions with CTR-ir cells were found in 12 of 14 GBM tumours (P < 0.05). Using confocal microscopy, CTR-ir cells were identified that were also positive for glial fibrillary acidic protein, nestin and CD133. Antibodies were verified using immunoblots and confocal microscopy of the Cercopithecus aethiops(COS)-7 transfectants. Immunoblots of membrane preparations from the CTR-positive cell lines demonstrated a major band (∼67 kDa) and minor band (∼52 kDa), but the intensity was reversed for the GBM cell line A172. In cultured A172 cells, functional studies demonstrated calcitonin stimulation of adenylyl cyclase and inhibition of extracellular-regulated kinase (ERK)1/2 phosphorylation. Conclusions:  The findings that (i) CTR was expressed by glioma cells in a majority of GBM tumours tested, (ii) CTR(+) /CD133(+) cells were identified and (iii) second messenger systems were functionally modified by calcitonin in A172 cells suggest that CTR might be a useful therapeutic target in GBM.
Peter J Wookey; Catriona A McLean; Peter Hwang; Sebastian G B Furness; Sandy Nguyen; Angela Kourakis; David L Hare; Jeffrey V Rosenfeld
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Publication Detail:
Type:  JOURNAL ARTICLE     Date:  2012-2-15
Journal Detail:
Title:  Histopathology     Volume:  -     ISSN:  1365-2559     ISO Abbreviation:  -     Publication Date:  2012 Feb 
Date Detail:
Created Date:  2012-2-16     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  7704136     Medline TA:  Histopathology     Country:  -    
Other Details:
Languages:  ENG     Pagination:  -     Citation Subset:  -    
Copyright Information:
© 2012 Blackwell Publishing Ltd.
Department of Medicine (at Austin Health, Heidelberg) Centre for Neuroscience, University of Melbourne, Melbourne Departments of Anatomical Pathology Neurosurgery, The Alfred Hospital, Prahran Drug Discovery Biology Laboratory, Monash Institute of Pharmaceutical Sciences and Department of Pharmacology, Monash University, Melbourne Department of Surgery, The Alfred Hospital, Monash University Medical School, Prahran, Vic., Australia.
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