| Title: |
High expression of XIAP and Bcl-2 may inhibit programmed cell death in glioblastomas |
| Authors: |
Tirapelli, Daniela Pretti da Cunha, Lustosa, Isis Lacrose, Menezes, Sarah Bomfim, Franco, Indira Maynart, Rodrigues, Andressa Romualdo, Peria, Fernanda Maris, Marinho, Alexandre Magno da Nóbrega, Serafini, Luciano Neder, Carlotti Jr, Carlos Gilberto, Tirapelli, Luís Fernando |
| Source: |
Arquivos de Neuro-Psiquiatria. December 2017 75(12) |
| Publisher Information: |
Academia Brasileira de Neurologia - ABNEURO, 2017. |
| Publication Year: |
2017 |
| Subject Terms: |
glioblastoma, apoptosis, X-linked inhibitor of apoptosis protein, B-cell lymphoma 2 |
| More Details: |
Glioblastoma (GBM) is the most malignant glioma and represents 29% of all brain tumors. Tumorigenesis is intimately connected with characteristics acquired in the physiologic pathway of cellular death. Objective: In the present study, the expression of anti-apoptotic (XIAP and Bcl-2) and apoptotic (cytochrome C, caspase 9, APAF-1), caspase 3 and the Smac/DIABLO genes related to the apoptosis pathway were evaluated in 30 samples of glioblastoma. Methods: The gene expression was evaluated in 30 glioblastomas (WHO grade IV) and compared to 10 white matter control samples with real-time PCR. Results and Conclusion: There were higher expressions of XIAP (p = 0.0032) and Bcl-2 (p = 0.0351) in the glioblastoma samples compared to the control samples of normal brain. These results raise the question of whether Bcl-2 and XIAP genes can be responsible for the inhibition of programmed cell death in glioblastomas. Moreover, they provide additional information capable of allowing the development of new target therapy strategies. |
| Document Type: |
article |
| File Description: |
text/html |
| Language: |
English |
| ISSN: |
0004-282X |
| DOI: |
10.1590/0004-282x20170156 |
| Access URL: |
http://old.scielo.br/scielo.php?script=sci_arttext&pid=S0004-282X2017001200875 |
| Rights: |
info:eu-repo/semantics/openAccess |
| Accession Number: |
edssci.S0004.282X2017001200875 |
| Database: |
SciELO |
