| Genetic and protein changes of E-cadherin in meningiomas. | |
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MedLine Citation:
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PMID: 19908067 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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PURPOSE: The molecular mechanisms and candidate genes involved in development of meningiomas still needs investigation and elucidation. METHODS: In the present study 60 meningiomas were analyzed regarding changes of tumor suppressor gene E-cadherin (CDH1), a component of adherens junction and an indirect modulator of the wnt signaling. Gene instability was tested by polymerase chain reaction/loss of heterozygosity (LOH) method. Protein expression was analyzed by immunohistochemistry. RESULTS: The results of our analysis showed altogether 32% of samples with LOH of the CDH1 gene. Interestingly, another type of genomic instability was detected; replication error-positive samples (RER+). Three out of 28 heterozygous samples were RER+ (11%). The instability is the result of impaired cellular mismatch repair. Fibrous and angiomatous cases showed higher percent of genetic changes, 67 and 75%, respectively. Immunostaining showed that overall 73% of samples had downregulation of E-cadherin expression. Intense downregulation of E-cadherin was noticed in tumors with grades II and III. Five out of nine samples with LOH were accompanied with the downregulation of E-cadherin protein expression (56%). One RER+ sample had lower expression of E-cadherin. We noticed that 36.4% of samples with lower E-cadherin expression had beta-catenin located in the nucleus. Also, 75% of samples with genomic instabilities had beta-catenin in the nucleus. Our findings demonstrated that there is significant association between the genetic changes of CDH1 and the nuclear localization of beta-catenin protein (chi(2) = 5.25, df = 1, P < 0.022). Beta-catenin was progressively upregulated from meningothelial to atypical, while 60% of anaplastic showed upregulation and nuclear localization of the protein. CONCLUSIONS: Our results suggest that genetic instabilities of the E-cadherin gene have a role in meningioma development and progression. Detected microsatellite instability indicates that mismatch repair may also be targeted in meningioma. |
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Authors:
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Nives Pe?ina-Slaus; Tamara Nikuseva Marti?; Adam Jakov Deak; Martina Zeljko; Reno Hras?an; Davor Tomas; Vesna Musani |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't Date: 2009-11-12 |
Journal Detail:
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Title: Journal of cancer research and clinical oncology Volume: 136 ISSN: 1432-1335 ISO Abbreviation: J. Cancer Res. Clin. Oncol. Publication Date: 2010 May |
Date Detail:
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Created Date: 2010-03-19 Completed Date: 2010-04-06 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 7902060 Medline TA: J Cancer Res Clin Oncol Country: Germany |
Other Details:
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Languages: eng Pagination: 695-702 Citation Subset: IM |
Affiliation:
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Croatian Institute for Brain Research, School of Medicine, University of Zagreb, Croatia. nina@mef.hr |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Adult Aged Cadherins / genetics*, metabolism Female Genomic Instability* Humans Loss of Heterozygosity Male Meningeal Neoplasms / genetics*, metabolism Meningioma / genetics*, metabolism Middle Aged beta Catenin / genetics |
| Chemical | |
Reg. No./Substance:
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0/Cadherins; 0/beta Catenin |
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