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Reduced levels of E-cadherin correlate with progression of corticotroph pituitary tumours.
- Source :
-
Clinical Endocrinology . Dec2011, Vol. 75 Issue 6, p811-818. 8p. 1 Color Photograph, 2 Charts, 2 Graphs. - Publication Year :
- 2011
-
Abstract
- Summary Objectives Loss of E-cadherin is an important marker of epithelial tumour progression. The aims of this study were to explore whether E-cadherin expression and localization correlate to corticotroph tumour progression, relate the expression of the E-cadherin gene ( CDH1) to immunohistochemical E-cadherin staining pattern, and study whether the E-cadherin levels were correlated to methylation status of the CDH1 promoter region. Design Immunohistochemical analyses of E-cadherin protein were performed, as was RT-qPCR of the CDH1 and the POMC genes. Methylation pattern of the promoter region of CDH1 was measured using pyrosequencing of bisulfite-treated DNA. Patients Forty-five patients operated at a tertiary referral centre in Oslo, Norway. Adenoma tissue sections and RNA samples from patients with verified Cushing's disease or Nelson's syndrome were collected. Measurements Expression of E-cadherin mRNA and protein in pituitary corticotroph adenomas and average percentage of methylated cytosines in a cytosine-phosphate-guanosine island of the CDH1 promoter. Results Correlations were observed between tumour progression and both nuclear expression of E-cadherin and reduced CDH1 mRNA. The E-cadherin expression was not determined by the methylation pattern of the CDH1 promoter. Conclusions Corticotroph tumour progression was associated with reduced expression of the epithelial marker E-cadherin. [ABSTRACT FROM AUTHOR]
- Subjects :
- *CADHERINS
*CANCER invasiveness
*ADENOMA
*METHYLATION
*MESSENGER RNA
Subjects
Details
- Language :
- English
- ISSN :
- 03000664
- Volume :
- 75
- Issue :
- 6
- Database :
- Academic Search Index
- Journal :
- Clinical Endocrinology
- Publication Type :
- Academic Journal
- Accession number :
- 67083727
- Full Text :
- https://doi.org/10.1111/j.1365-2265.2011.04109.x