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E-cadherin as potential biomarker for progression of intracranial meningioma (CROSBI ID 683750)

Prilog sa skupa u zborniku | sažetak izlaganja sa skupa | međunarodna recenzija

Brlek, Petar ; Bukovac, Anja ; Kafka, Anja ; Pećina- Šlaus, Nives E-cadherin as potential biomarker for progression of intracranial meningioma // RECOOP - Frigyes Korányi Science Forum 2018. 2018. str. 38-38

Podaci o odgovornosti

Brlek, Petar ; Bukovac, Anja ; Kafka, Anja ; Pećina- Šlaus, Nives

engleski

E-cadherin as potential biomarker for progression of intracranial meningioma

Introduction: Recent studies have shown that epithelial-mesenchymal transition (EMT), biological process necessary for embryogenesis, could also be involved in invasiveness of different tumor types. One of the prominent features of EMT is loss of expression of E- cadherin. In our research we wanted to verify if loss of E-cadherin could be a potential marker of the molecular changes responsible for the control of cellular mobility and therefor for progression of intracranial meningioma. Methods: We analysed genetic changes of E- cadherin gene (CDH1) and its protein expression in 45 samples of human meningioma with different grades of malignancy. Genetic alternations of CDH1 gene (loss of heterozygosity, microsatellite instability) were tested by polymerase chain reaction (PCR) using microsatellite marker D16S3025 and analysed by electrophoresis on Spreadex gels. To assess and localize E-cadherin expression, we used DAB- labeled immunohistochemical reaction using streptavidin horseradish peroxidase/DAB (EnVisionTM, Dako REALTM) and specific monoclonal antibody E- cadherin. Results: The results on CDH1 changes showed that genetic changes of E-cadherin were present in a portion of meningioma (9% of samples showed LOH, 13% of samples showed MSI and 4% of samples showed LOH and MSI). Protein expression was still high or moderate in samples demonstrating genetic changes, but varied in samples with different grades. Two atypical meningiomas lacked E- cadherin expression. Discussion: Samples with genetic changes did not demonstrate low expression of E-cadherin. That could be explained with a second functional allele in the genome. Some samples with higher grades of malignancy didn’t express E-cadherin, partially confirming our hypothesis of E-cadherin involvement in meningioma progression. Conclusion: To confirm that our findings can indicate the involvement of E-cadherin expression reduction in meningioma progression, experiments and statistical analysis should be performed on higher number of meningioma with grades II and III. After additional future analyses our findings could be useful as potential biomarkers of cellular mobility of invasive intracranial meningiomas.

E-kadherin ; loss of heterozygosity ; MSI ; meningioma

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Podaci o prilogu

38-38.

2018.

objavljeno

Podaci o matičnoj publikaciji

RECOOP - Frigyes Korányi Science Forum 2018

978-615-00-1489-0

Podaci o skupu

Student Conference RECOOP - Frigyes Korányi Science Forum 2018

poster

09.04.2018-09.04.2018

Budimpešta, Mađarska

Povezanost rada

Biologija, Temeljne medicinske znanosti